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1
Amirah, Farah. "The neurochemical underpinnings of autism spectrum disorder." International Journal of Clinical Medical Research 3, no. 1 (January 22, 2025): 16–17. https://doi.org/10.61466/ijcmr3010004.
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Autism spectrum disorder encompasses a range of neurobehavioral and neurodevelopmental conditions marked by deficits in social interaction and communication, as well as restricted and repetitive behaviors or interests, alongside atypical sensory processing. Environmental, immunological, genetic, and epigenetic factors contribute to the pathophysiology of autism, triggering neuroanatomical and neurochemical changes early in central nervous system development. Numerous neurochemical pathways contribute to the etiology of autism spectrum disorder; however, the interactions among these intricate networks and their role in the emergence of core autism symptoms remain poorly understood. Additional research on neurochemical changes in autism is essential to elucidate the early neurodevelopmental differences that contribute to the significant heterogeneity of autism spectrum disorder, thereby informing new strategies for treatment and prevention.
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Khani, Abbas, and Gregor Rainer. "Neural and neurochemical basis of reinforcement-guided decision making." Journal of Neurophysiology 116, no. 2 (August 1, 2016): 724–41. http://dx.doi.org/10.1152/jn.01113.2015.
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Decision making is an adaptive behavior that takes into account several internal and external input variables and leads to the choice of a course of action over other available and often competing alternatives. While it has been studied in diverse fields ranging from mathematics, economics, ecology, and ethology to psychology and neuroscience, recent cross talk among perspectives from different fields has yielded novel descriptions of decision processes. Reinforcement-guided decision making models are based on economic and reinforcement learning theories, and their focus is on the maximization of acquired benefit over a defined period of time. Studies based on reinforcement-guided decision making have implicated a large network of neural circuits across the brain. This network includes a wide range of cortical (e.g., orbitofrontal cortex and anterior cingulate cortex) and subcortical (e.g., nucleus accumbens and subthalamic nucleus) brain areas and uses several neurotransmitter systems (e.g., dopaminergic and serotonergic systems) to communicate and process decision-related information. This review discusses distinct as well as overlapping contributions of these networks and neurotransmitter systems to the processing of decision making. We end the review by touching on neural circuitry and neuromodulatory regulation of exploratory decision making.
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Marotta, Rosa, Maria C. Risoleo, Giovanni Messina, Lucia Parisi, Marco Carotenuto, Luigi Vetri, and Michele Roccella. "The Neurochemistry of Autism." Brain Sciences 10, no. 3 (March 13, 2020): 163. http://dx.doi.org/10.3390/brainsci10030163.
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Autism spectrum disorder (ASD) refers to complex neurobehavioral and neurodevelopmental conditions characterized by impaired social interaction and communication, restricted and repetitive patterns of behavior or interests, and altered sensory processing. Environmental, immunological, genetic, and epigenetic factors are implicated in the pathophysiology of autism and provoke the occurrence of neuroanatomical and neurochemical events relatively early in the development of the central nervous system. Many neurochemical pathways are involved in determining ASD; however, how these complex networks interact and cause the onset of the core symptoms of autism remains unclear. Further studies on neurochemical alterations in autism are necessary to clarify the early neurodevelopmental variations behind the enormous heterogeneity of autism spectrum disorder, and therefore lead to new approaches for the treatment and prevention of autism. In this review, we aim to delineate the state-of-the-art main research findings about the neurochemical alterations in autism etiology, and focuses on gamma aminobutyric acid (GABA) and glutamate, serotonin, dopamine, N-acetyl aspartate, oxytocin and arginine-vasopressin, melatonin, vitamin D, orexin, endogenous opioids, and acetylcholine. We also aim to suggest a possible related therapeutic approach that could improve the quality of ASD interventions. Over one hundred references were collected through electronic database searching in Medline and EMBASE (Ovid), Scopus (Elsevier), ERIC (Proquest), PubMed, and the Web of Science (ISI).
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Jiménez-Jiménez, Félix, Hortensia Alonso-Navarro, Elena García-Martín, and José Agúndez. "Neurochemical Features of Rem Sleep Behaviour Disorder." Journal of Personalized Medicine 11, no. 9 (August 31, 2021): 880. http://dx.doi.org/10.3390/jpm11090880.
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Dopaminergic deficiency, shown by many studies using functional neuroimaging with Single Photon Emission Computerized Tomography (SPECT) and Positron Emission Tomography (PET), is the most consistent neurochemical feature of rapid eye movement (REM) sleep behaviour disorder (RBD) and, together with transcranial ultrasonography, and determination of alpha-synuclein in certain tissues, should be considered as a reliable marker for the phenoconversion of idiopathic RBD (iRBD) to a synucleopathy (Parkinson’s disease –PD- or Lewy body dementia -LBD). The possible role in the pathogenesis of RBD of other neurotransmitters such as noradrenaline, acetylcholine, and excitatory and inhibitory neurotransmitters; hormones such as melatonin, and proinflammatory factors have also been suggested by recent reports. In general, brain perfusion and brain glucose metabolism studies have shown patterns resembling partially those of PD and LBD. Finally, the results of structural and functional MRI suggest the presence of structural changes in deep gray matter nuclei, cortical gray matter atrophy, and alterations in the functional connectivity within the basal ganglia, the cortico-striatal, and the cortico-cortical networks, but they should be considered as preliminary.
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Schwarz, Adam J., Alessandro Gozzi, Alessandro Chessa, and Angelo Bifone. "Voxel Scale Complex Networks of Functional Connectivity in the Rat Brain: Neurochemical State Dependence of Global and Local Topological Properties." Computational and Mathematical Methods in Medicine 2012 (2012): 1–15. http://dx.doi.org/10.1155/2012/615709.
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Network analysis of functional imaging data reveals emergent features of the brain as a function of its topological properties. However, the brain is not a homogeneous network, and the dependence of functional connectivity parameters on neuroanatomical substrate and parcellation scale is a key issue. Moreover, the extent to which these topological properties depend on underlying neurochemical changes remains unclear. In the present study, we investigated both global statistical properties and the local, voxel-scale distribution of connectivity parameters of the rat brain. Different neurotransmitter systems were stimulated by pharmacological challenge (d-amphetamine, fluoxetine, and nicotine) to discriminate between stimulus-specific functional connectivity and more general features of the rat brain architecture. Although global connectivity parameters were similar, mapping of local connectivity parameters at high spatial resolution revealed strong neuroanatomical dependence of functional connectivity in the rat brain, with clear differentiation between the neocortex and older brain regions. Localized foci of high functional connectivity independent of drug challenge were found in the sensorimotor cortices, consistent with the high neuronal connectivity in these regions. Conversely, the topological properties and node roles in subcortical regions varied with neurochemical state and were dependent on the specific dynamics of the different functional processes elicited.
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Frisaldi, Elisa, Alessandro Piedimonte, and Fabrizio Benedetti. "Placebo and Nocebo Effects: A Complex Interplay Between Psychological Factors and Neurochemical Networks." American Journal of Clinical Hypnosis 57, no. 3 (January 13, 2015): 267–84. http://dx.doi.org/10.1080/00029157.2014.976785.
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Brodowicz, Justyna, Edmund Przegaliński, Christian P. Müller, and Malgorzata Filip. "Ceramide and Its Related Neurochemical Networks as Targets for Some Brain Disorder Therapies." Neurotoxicity Research 33, no. 2 (August 25, 2017): 474–84. http://dx.doi.org/10.1007/s12640-017-9798-6.
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Samardžija, Bobana, Milan Petrović, Beti Zaharija, Marta Medija, Ana Meštrović, Nicholas J. Bradshaw, Ana Filošević Vujnović, and Rozi Andretić Waldowski. "Transgenic Drosophila melanogaster Carrying a Human Full-Length DISC1 Construct (UAS-hflDISC1) Showing Effects on Social Interaction Networks." Current Issues in Molecular Biology 46, no. 8 (August 3, 2024): 8526–49. http://dx.doi.org/10.3390/cimb46080502.
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Disrupted in Schizophrenia 1 (DISC1) is a scaffold protein implicated in major mental illnesses including schizophrenia, with a significant negative impact on social life. To investigate if DISC1 affects social interactions in Drosophila melanogaster, we created transgenic flies with second or third chromosome insertions of the human full-length DISC1 (hflDISC1) gene fused to a UAS promotor (UAS-hflDISC1). Initial characterization of the insertion lines showed unexpected endogenous expression of the DISC1 protein that led to various behavioral and neurochemical phenotypes. Social interaction network (SIN) analysis showed altered social dynamics and organizational structures. This was in agreement with the altered levels of the locomotor activity of individual flies monitored for 24 h. Together with a decreased ability to climb vertical surfaces, the observed phenotypes indicate altered motor functions that could be due to a change in the function of the motor neurons and/or central brain. The changes in social behavior and motor function suggest that the inserted hflDISC1 gene influences nervous system functioning that parallels symptoms of DISC1-related mental diseases in humans. Furthermore, neurochemical analyses of transgenic lines revealed increased levels of hydrogen peroxide and decreased levels of glutathione, indicating an impact of DISC1 on the dynamics of redox regulation, similar to that reported in transgenic mammals. Future studies are needed to address the localization of DISC1 expression and to address how the redox parameter changes correlate with the observed behavioral changes.
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Ziminski, Joseph J., Polytimi Frangou, Vasilis M. Karlaftis, Uzay Emir, and Zoe Kourtzi. "Microstructural and neurochemical plasticity mechanisms interact to enhance human perceptual decision-making." PLOS Biology 21, no. 3 (March 10, 2023): e3002029. http://dx.doi.org/10.1371/journal.pbio.3002029.
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Experience and training are known to boost our skills and mold the brain’s organization and function. Yet, structural plasticity and functional neurotransmission are typically studied at different scales (large-scale networks, local circuits), limiting our understanding of the adaptive interactions that support learning of complex cognitive skills in the adult brain. Here, we employ multimodal brain imaging to investigate the link between microstructural (myelination) and neurochemical (GABAergic) plasticity for decision-making. We test (in males, due to potential confounding menstrual cycle effects on GABA measurements in females) for changes in MRI-measured myelin, GABA, and functional connectivity before versus after training on a perceptual decision task that involves identifying targets in clutter. We demonstrate that training alters subcortical (pulvinar, hippocampus) myelination and its functional connectivity to visual cortex and relates to decreased visual cortex GABAergic inhibition. Modeling interactions between MRI measures of myelin, GABA, and functional connectivity indicates that pulvinar myelin plasticity interacts—through thalamocortical connectivity—with GABAergic inhibition in visual cortex to support learning. Our findings propose a dynamic interplay of adaptive microstructural and neurochemical plasticity in subcortico-cortical circuits that supports learning for optimized decision-making in the adult human brain.
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De Pascalis, Vilfredo. "Brain Functional Correlates of Resting Hypnosis and Hypnotizability: A Review." Brain Sciences 14, no. 2 (January 24, 2024): 115. http://dx.doi.org/10.3390/brainsci14020115.
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This comprehensive review delves into the cognitive neuroscience of hypnosis and variations in hypnotizability by examining research employing functional magnetic resonance imaging (fMRI), positron emission tomography (PET), and electroencephalography (EEG) methods. Key focus areas include functional brain imaging correlations in hypnosis, EEG band oscillations as indicators of hypnotic states, alterations in EEG functional connectivity during hypnosis and wakefulness, drawing critical conclusions, and suggesting future research directions. The reviewed functional connectivity findings support the notion that disruptions in the available integration between different components of the executive control network during hypnosis may correspond to altered subjective appraisals of the agency during the hypnotic response, as per dissociated and cold control theories of hypnosis. A promising exploration avenue involves investigating how frontal lobes’ neurochemical and aperiodic components of the EEG activity at waking-rest are linked to individual differences in hypnotizability. Future studies investigating the effects of hypnosis on brain function should prioritize examining distinctive activation patterns across various neural networks.
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McCarty, Patrick J., Andrew R. Pines, Bethany L. Sussman, Sarah N. Wyckoff, Amanda Jensen, Raymond Bunch, Varina L. Boerwinkle, and Richard E. Frye. "Resting State Functional Magnetic Resonance Imaging Elucidates Neurotransmitter Deficiency in Autism Spectrum Disorder." Journal of Personalized Medicine 11, no. 10 (September 28, 2021): 969. http://dx.doi.org/10.3390/jpm11100969.
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Resting-state functional magnetic resonance imaging provides dynamic insight into the functional organization of the brains’ intrinsic activity at rest. The emergence of resting-state functional magnetic resonance imaging in both the clinical and research settings may be attributed to recent advancements in statistical techniques, non-invasiveness and enhanced spatiotemporal resolution compared to other neuroimaging modalities, and the capability to identify and characterize deep brain structures and networks. In this report we describe a 16-year-old female patient with autism spectrum disorder who underwent resting-state functional magnetic resonance imaging due to late regression. Imaging revealed deactivated networks in deep brain structures involved in monoamine synthesis. Monoamine neurotransmitter deficits were confirmed by cerebrospinal fluid analysis. This case suggests that resting-state functional magnetic resonance imaging may have clinical utility as a non-invasive biomarker of central nervous system neurochemical alterations by measuring the function of neurotransmitter-driven networks. Use of this technology can accelerate and increase the accuracy of selecting appropriate therapeutic agents for patients with neurological and neurodevelopmental disorders.
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Harvey, John, and Thomas Heinbockel. "Neuromodulation of Synaptic Transmission in the Main Olfactory Bulb." International Journal of Environmental Research and Public Health 15, no. 10 (October 8, 2018): 2194. http://dx.doi.org/10.3390/ijerph15102194.
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A major step in our understanding of brain function is to determine how neural circuits are altered in their function by signaling molecules or neuromodulators. Neuromodulation is the neurochemical process that modifies the computations performed by a neuron or network based on changing the functional needs or behavioral state of the subject. These modulations have the effect of altering the responsivity to synaptic inputs. Early sensory processing areas, such as the main olfactory bulb, provide an accessible window for investigating how neuromodulation regulates the functional states of neural networks and influences how we process sensory information. Olfaction is an attractive model system in this regard because of its relative simplicity and because it links primary olfactory sensory neurons to higher olfactory and associational networks. Likewise, centrifugal fibers from higher order brain centers target neurons in the main olfactory bulb to regulate synaptic processing. The neuromodulatory systems that provide regulatory inputs and play important roles in olfactory sensory processing and behaviors include the endocannabinoid system, the dopaminergic system, the cholinergic system, the noradrenergic system and the serotonergic system. Here, we present a brief survey of neuromodulation of olfactory signals in the main olfactory bulb with an emphasis on the endocannabinoid system.
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Staniloiu, A., and H. J. Markowitsch. "FC29-04 - Gene-brain -environment interactions in violent behavior." European Psychiatry 26, S2 (March 2011): 1980. http://dx.doi.org/10.1016/s0924-9338(11)73683-5.
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IntroductionThe prediction, prevention and treatment of violence pose several challenges that are partly due to incompletely described neurobiological underpinnings of human violent behavior.ObjectivesThis work's objectives are establishing greater recognition of the neurochemical substrates of violent behavior and importance of the gene-environment interplay in the development of violence, distinguishing the components of the functional neural networks involved in violent behavior and facilitating the interpretation of relations between brain damage and alterations in social behavior from a perspective that takes into account variables such as developmental phase, brain-environment interactions and neuroplasticity.AimsWe provide an overview of the neurobiological underpinnings of violence and the roles and advantages of using static and functional brain imaging in studying violent behavior.MethodsA comprehensive review of the scientific literature on the neurobiology of violence was performed. A theoretical framework for the possible role of epigenetic factors in mediating the predisposition for violence is advanced.ResultsResearch data from various fields (such as genetics, cognitive and affective neurosciences, static and functional neuroimaging) suggest that the predisposition for violent behavior is influenced by both genetic and environmental factors. Epigenetic mechanisms underlying lasting environmentally-induced modifications in gene expression have recently been implicated in the pathogeny of various psychiatric and non-psychiatric diseases and social behavior disturbances.ConclusionsThe genetic, neurochemical and neuroimaging findings from various studies emphasize the complex role of the gene-environment interplay in the pathogenesis of violence and open a path of hope for the development and optimal timing of violence prevention strategies.
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Skolariki, Konstantina, Aristidis G. Vrahatis, Marios G. Krokidis, Themis P. Exarchos, and Panagiotis Vlamos. "Assessing and Modelling of Post-Traumatic Stress Disorder Using Molecular and Functional Biomarkers." Biology 12, no. 8 (July 26, 2023): 1050. http://dx.doi.org/10.3390/biology12081050.
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Post-traumatic stress disorder (PTSD) is a complex psychological disorder that develops following exposure to traumatic events. PTSD is influenced by catalytic factors such as dysregulated hypothalamic-pituitary-adrenal (HPA) axis, neurotransmitter imbalances, and oxidative stress. Genetic variations may act as important catalysts, impacting neurochemical signaling, synaptic plasticity, and stress response systems. Understanding the intricate gene networks and their interactions is vital for comprehending the underlying mechanisms of PTSD. Focusing on the catalytic factors of PTSD is essential because they provide valuable insights into the underlying mechanisms of the disorder. By understanding these factors and their interplay, researchers may uncover potential targets for interventions and therapies, leading to more effective and personalized treatments for individuals with PTSD. The aforementioned gene networks, composed of specific genes associated with the disorder, provide a comprehensive view of the molecular pathways and regulatory mechanisms involved in PTSD. Through this study valuable insights into the disorder’s underlying mechanisms and opening avenues for effective treatments, personalized interventions, and the development of biomarkers for early detection and monitoring are provided.
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van Vugt, F. T., J. Near, T. Hennessy, J. Doyon, and D. J. Ostry. "Early stages of sensorimotor map acquisition: neurochemical signature in primary motor cortex and its relation to functional connectivity." Journal of Neurophysiology 124, no. 6 (December 1, 2020): 1615–24. http://dx.doi.org/10.1152/jn.00285.2020.
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Learning the mapping between movements and their sensory effects is a necessary step in the early stages of sensorimotor learning. There is evidence showing which brain areas are involved in early motor learning, but their role remains uncertain. Here, we show that GABA, a neurotransmitter linked to inhibitory processing, rises during and after learning and is involved in ongoing changes in resting-state networks.
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Bazyan, A. S., and G. van Luijtelaar. "Neurochemical and Behavioral Features in Genetic Absence Epilepsy and in Acutely Induced Absence Seizures." ISRN Neurology 2013 (May 7, 2013): 1–48. http://dx.doi.org/10.1155/2013/875834.
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The absence epilepsy typical electroencephalographic pattern of sharp spikes and slow waves (SWDs) is considered to be due to an interaction of an initiation site in the cortex and a resonant circuit in the thalamus. The hyperpolarization-activated cyclic nucleotide-gated cationic Ih pacemaker channels (HCN) play an important role in the enhanced cortical excitability. The role of thalamic HCN in SWD occurrence is less clear. Absence epilepsy in the WAG/Rij strain is accompanied by deficiency of the activity of dopaminergic system, which weakens the formation of an emotional positive state, causes depression-like symptoms, and counteracts learning and memory processes. It also enhances GABAA receptor activity in the striatum, globus pallidus, and reticular thalamic nucleus, causing a rise of SWD activity in the cortico-thalamo-cortical networks. One of the reasons for the occurrence of absences is that several genes coding of GABAA receptors are mutated. The question arises: what the role of DA receptors is. Two mechanisms that cause an infringement of the function of DA receptors in this genetic absence epilepsy model are proposed.
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Aydin, Mehmet Dumlu, Aybike Aydin, Ozgur Caglar, Muhammed Enes Aydin, Erdem Karadeniz, Kemal Alp Nalci, and Rabia Demirtas. "New description of vagal nerve commanted intrapancreatic taste buds and blood glucose level: An experimental analysis." BioImpacts 11, no. 3 (July 8, 2020): 181–85. http://dx.doi.org/10.34172/bi.2021.26.
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Introduction: There have been thousands of neurochemical mechanism about blood glucose level regulation, but intrapancreatic taste buds and their roles in blood glucose level has not been described. We aimed to investigate if there are taste buds cored neural networks in the pancreas, and there is any relationship between blood glucose levels. Methods: This examination was done on 32 chosen rats with their glucose levels. Animals are divided into owned blood glucose levels. If mean glucose levels were equal to 105 ± 10 mg/dL accepted as euglycemic (G-I; n = 14), 142 ± 18 mg/dL values accepted as hyperglycemic (G-II; n = 9) and 89 ± 9 mg/dL accepted as hypoglycemic (G-III; n = 9). After the experiment, animals were sacrificed under general anesthesia. Their pancreatic tissues were examined histological methods and numbers of newly described taste bud networks analyzed by Stereological methods. Results compared with Mann-Whitney U test P < 0.005 considered as significant. Results: The mean normal blood glucose level (mg/dL) and taste bud network densities of per cm3 were: 105 ± 10 mg/dL; 156±21 in G-I; 142 ± 18 mg/dL and 95 ± 14 in G-II and 89 ± 9 mg/dL and 232 ± 34 in G-III. P values as follows: P < 0.001 of G-II/G-I; P < 0.005 of G-III/G-I and P < 0.0001 of G-III/G-II. We detected periarterial located taste buds like cell clusters and peripherally located ganglia connected with Langerhans cells via thin nerve fibers. There was an inverse relationship between the number of taste buds networks and blood glucose level. Conclusion: Newly described intrapancreatic taste buds may have an important role in the regulation of blood glucose level.
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Kozlova, Elena V., Matthew C. Valdez, Maximillian E. Denys, Anthony E. Bishay, Julia M. Krum, Kayhon M. Rabbani, Valeria Carrillo, et al. "Persistent autism-relevant behavioral phenotype and social neuropeptide alterations in female mice offspring induced by maternal transfer of PBDE congeners in the commercial mixture DE-71." Archives of Toxicology 96, no. 1 (October 23, 2021): 335–65. http://dx.doi.org/10.1007/s00204-021-03163-4.
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AbstractPolybrominated diphenyl ethers (PBDEs) are ubiquitous persistent organic pollutants (POPs) that are known neuroendocrine disrupting chemicals with adverse neurodevelopmental effects. PBDEs may act as risk factors for autism spectrum disorders (ASD), characterized by abnormal psychosocial functioning, although direct evidence is currently lacking. Using a translational exposure model, we tested the hypothesis that maternal transfer of a commercial mixture of PBDEs, DE-71, produces ASD-relevant behavioral and neurochemical deficits in female offspring. C57Bl6/N mouse dams (F0) were exposed to DE-71 via oral administration of 0 (VEH/CON), 0.1 (L-DE-71) or 0.4 (H-DE-71) mg/kg bw/d from 3 wk prior to gestation through end of lactation. Mass spectrometry analysis indicated in utero and lactational transfer of PBDEs (in ppb) to F1 female offspring brain tissue at postnatal day (PND) 15 which was reduced by PND 110. Neurobehavioral testing of social novelty preference (SNP) and social recognition memory (SRM) revealed that adult L-DE-71 F1 offspring display deficient short- and long-term SRM, in the absence of reduced sociability, and increased repetitive behavior. These effects were concomitant with reduced olfactory discrimination of social odors. Additionally, L-DE-71 exposure also altered short-term novel object recognition memory but not anxiety or depressive-like behavior. Moreover, F1 L-DE-71 displayed downregulated mRNA transcripts for oxytocin (Oxt) in the bed nucleus of the stria terminalis (BNST) and supraoptic nucleus, and vasopressin (Avp) in the BNST and upregulated Avp1ar in BNST, and Oxtr in the paraventricular nucleus. Our work demonstrates that developmental PBDE exposure produces ASD-relevant neurochemical, olfactory processing and behavioral phenotypes that may result from early neurodevelopmental reprogramming within central social and memory networks.
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Tremere, Liisa A., Kaiping Burrows, Jin-Kwon Jeong, and Raphael Pinaud. "Organization of Estrogen-Associated Circuits in the Mouse Primary Auditory Cortex." Journal of Experimental Neuroscience 5 (January 2011): JEN.S7744. http://dx.doi.org/10.4137/jen.s7744.
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Sex steroid hormones influence the perceptual processing of sensory signals in vertebrates. In particular, decades of research have shown that circulating levels of estrogen correlate with hearing function. The mechanisms and sites of action supporting this sensory-neuroendocrine modulation, however, remain unknown. Here we combined a molecular cloning strategy, fluorescence in-situ hybridization and unbiased quantification methods to show that estrogen-producing and -sensitive neurons heavily populate the adult mouse primary auditory cortex (AI). We also show that auditory experience in freely-behaving animals engages estrogen-producing and -sensitive neurons in AI. These estrogen-associated networks are greatly stable, and do not quantitatively change as a result of acute episodes of sensory experience. We further demonstrate the neurochemical identity of estrogen-producing and estrogen-sensitive neurons in AI and show that these cell populations are phenotypically distinct. Our findings provide the first direct demonstration that estrogen-associated circuits are highly prevalent and engaged by sensory experience in the mouse auditory cortex, and suggest that previous correlations between estrogen levels and hearing function may be related to brain-generated hormone production. Finally, our findings suggest that estrogenic modulation may be a central component of the operational framework of central auditory networks.
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Nurmatova , D. A., N. G. Zhukova , Z. F. Sayfitdinkhuzhaev , and J. M. Okhunbaev . "Morphometric Characteristics of Cerebral Structures in Gilles De La Tourette Syndrome." Personalized Psychiatry and Neurology 5, no. 1 (March 17, 2025): 2–9. https://doi.org/10.52667/2712-9179-2025-5-1-2-9.
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Tic disorders, in particular Tourette syndrome, are a neurodevelopmental disorder common in children. Clinical manifestations of these disorders vary significantly depending on individual characteristics, age, gender, and the presence or absence of comorbidities. The pathophysiology of these disorders is believed to include a combination of genetic, environmental, psychological, immunological, and neurobiological factors. From the point of view of fundamental neurophysiology, Tourette syndrome is associated with a neurochemical imbalance of monoamines and morphometric changes affecting, in particular, neural networks that provide motor acts: the basal ganglia, thalamus, and cingulate cortex. To date, numerous studies have demonstrated the involvement of many more brain areas, such as the prefrontal cortex and cerebellum. This article presents the latest studies affecting the morphometric features of cerebral structures in patients with Tourette syndrome. During the analysis of the literature, a connection was revealed between the clinical manifestations of the disease and the morphometric characteristics of the basal ganglia, thalamus, cerebellum, cingulate gyrus and prefrontal cortex of patients with Gilles de la Tourette syndrome.
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Tan, Chao, Elaine M. Robbins, Bingchen Wu, and Xinyan Tracy Cui. "Recent Advances in In Vivo Neurochemical Monitoring." Micromachines 12, no. 2 (February 18, 2021): 208. http://dx.doi.org/10.3390/mi12020208.
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The brain is a complex network that accounts for only 5% of human mass but consumes 20% of our energy. Uncovering the mysteries of the brain’s functions in motion, memory, learning, behavior, and mental health remains a hot but challenging topic. Neurochemicals in the brain, such as neurotransmitters, neuromodulators, gliotransmitters, hormones, and metabolism substrates and products, play vital roles in mediating and modulating normal brain function, and their abnormal release or imbalanced concentrations can cause various diseases, such as epilepsy, Alzheimer’s disease, and Parkinson’s disease. A wide range of techniques have been used to probe the concentrations of neurochemicals under normal, stimulated, diseased, and drug-induced conditions in order to understand the neurochemistry of drug mechanisms and develop diagnostic tools or therapies. Recent advancements in detection methods, device fabrication, and new materials have resulted in the development of neurochemical sensors with improved performance. However, direct in vivo measurements require a robust sensor that is highly sensitive and selective with minimal fouling and reduced inflammatory foreign body responses. Here, we review recent advances in neurochemical sensor development for in vivo studies, with a focus on electrochemical and optical probes. Other alternative methods are also compared. We discuss in detail the in vivo challenges for these methods and provide an outlook for future directions.
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Voronkov, Dmitry N., Alla V. Stavrovskaya, Anastasia S. Guschina, Artyom S. Olshansky, Olga S. Lebedeva, Artyom V. Eremeev, and Maria A. Lagarkova. "Morphological Characterization of Astrocytes in a Xenograft of Human iPSC-Derived Neural Precursor Cells." Acta Naturae 14, no. 3 (October 29, 2022): 100–108. http://dx.doi.org/10.32607/actanaturae.11710.
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Transplantation of a mixed astrocyte and neuron culture is of interest in the development of cell therapies for neurodegenerative diseases. In this case, an assessment of engraftment requires a detailed morphological characterization, in particular an analysis of the neuronal and glial populations. In the experiment performed, human iPSC-derived neural progenitors transplanted into a rat striatum produced a mixed neuron and astrocyte population in vivo by the sixth month after transplantation. The morphological characteristics and neurochemical profile of the xenografted astrocytes were similar to those of mature human astroglia. Unlike neurons, astrocytes migrated to the surrounding structures and the density and pattern of their distribution in the striatum and cerebral cortex differed, which indicates that the microenvironment affects human glia integration. The graft was characterized by the zonal features of glial cell morphology, which was a reflection of cell maturation in the central area, glial shaft formation around the transplanted neurons, and migration to the surrounding structures.
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Zaporozhets, Eugene, Kristine C. Cowley, and Brian J. Schmidt. "Neurochemical excitation of propriospinal neurons facilitates locomotor command signal transmission in the lesioned spinal cord." Journal of Neurophysiology 105, no. 6 (June 2011): 2818–29. http://dx.doi.org/10.1152/jn.00917.2010.
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Previous studies of the in vitro neonatal rat brain stem-spinal cord showed that propriospinal relays contribute to descending transmission of a supraspinal command signal that is capable of activating locomotion. Using the same preparation, the present series examines whether enhanced excitation of thoracic propriospinal neurons facilitates propagation of the locomotor command signal in the lesioned spinal cord. First, we identified neurotransmitters contributing to normal endogenous propriospinal transmission of the locomotor command signal by testing the effect of receptor antagonists applied to cervicothoracic segments during brain stem-induced locomotor-like activity. Spinal cords were either intact or contained staggered bilateral hemisections located at right T1/T2 and left T10/T11 junctions designed to abolish direct long-projecting bulbospinal axons. Serotonergic, noradrenergic, dopaminergic, and glutamatergic, but not cholinergic, receptor antagonists blocked locomotor-like activity. Approximately 73% of preparations with staggered bilateral hemisections failed to generate locomotor-like activity in response to electrical stimulation of the brain stem alone; such preparations were used to test the effect of neuroactive substances applied to thoracic segments (bath barriers placed at T3 and T9) during brain stem stimulation. The percentage of preparations developing locomotor-like activity was as follows: 5-HT (43%), 5-HT/ N-methyl-d-aspartate (NMDA; 33%), quipazine (42%), 8-hydroxy-2-(di- n-propylamino)tetralin (20%), methoxamine (45%), and elevated bath K+ concentration (29%). Combined norepinephrine and dopamine increased the success rate (67%) compared with the use of either agent alone (4 and 7%, respectively). NMDA, Mg2+ ion removal, clonidine, and acetylcholine were ineffective. The results provide proof of principle that artificial excitation of thoracic propriospinal neurons can improve supraspinal control over hindlimb locomotor networks in the lesioned spinal cord.
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Graf, Heiko, Birgit Abler, Antonie Hartmann, Coraline D. Metzger, and Martin Walter. "Modulation of attention network activation under antidepressant agents in healthy subjects." International Journal of Neuropsychopharmacology 16, no. 6 (July 1, 2013): 1219–30. http://dx.doi.org/10.1017/s1461145712001368.
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Abstract While antidepressants are supposed to exert similar effects on mood and drive via various mechanisms of action, diverging effects are observed regarding side-effects and accordingly on neural correlates of motivation, emotion, reward and salient stimuli processing as a function of the drugs impact on neurotransmission. In the context of erotic stimulation, a unidirectional modulation of attentional functioning despite opposite effects on sexual arousal has been suggested for the selective serotonin reuptake-inhibitor (SSRI) paroxetine and the selective dopamine and noradrenaline reuptake-inhibitor (SDNRI) bupropion. To further elucidate the effects of antidepressant-related alterations of neural attention networks, we investigated 18 healthy males under subchronic administration (7 d) of paroxetine (20 mg), bupropion (150 mg) and placebo within a randomized placebo-controlled cross-over double-blind functional magnetic resonance imaging (fMRI) design during an established preceding attention task. Neuropsychological effects beyond the fMRI-paradigm were assessed by measuring alertness and divided attention. Comparing preceding attention periods of salient vs. neutral pictures, we revealed congruent effects of both drugs vs. placebo within the anterior midcingulate cortex, dorsolateral prefrontal cortex, anterior prefrontal cortex, superior temporal gyrus, anterior insula and the thalamus. Relatively decreased activation in this network was paralleled by slower reaction times in the divided attention task in both verum conditions compared to placebo. Our results suggest similar effects of antidepressant treatments on behavioural and neural attentional functioning by diverging neurochemical pathways. Concurrent alterations of brain regions within a fronto-parietal and cingulo-opercular attention network for top-down control could point to basic neural mechanisms of antidepressant action irrespective of receptor profiles.
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Bijanki, Kelly R., Yagna J. Pathak, Ricardo A. Najera, Eric A. Storch, Wayne K. Goodman, H. Blair Simpson, and Sameer A. Sheth. "Defining functional brain networks underlying obsessive–compulsive disorder (OCD) using treatment-induced neuroimaging changes: a systematic review of the literature." Journal of Neurology, Neurosurgery & Psychiatry 92, no. 7 (April 27, 2021): 776–86. http://dx.doi.org/10.1136/jnnp-2020-324478.
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Approximately 2%–3% of the population suffers from obsessive–compulsive disorder (OCD). Several brain regions have been implicated in the pathophysiology of OCD, but their various contributions remain unclear. We examined changes in structural and functional neuroimaging before and after a variety of therapeutic interventions as an index into identifying the underlying networks involved. We identified 64 studies from 1990 to 2020 comparing pretreatment and post-treatment imaging of patients with OCD, including metabolic and perfusion, neurochemical, structural, functional and connectivity-based modalities. Treatment class included pharmacotherapy, cognitive–behavioural therapy/exposure and response prevention, stereotactic lesions, deep brain stimulation and transcranial magnetic stimulation. Changes in several brain regions are consistent and correspond with treatment response despite the heterogeneity in treatments and neuroimaging modalities. Most notable are decreases in metabolism and perfusion of the caudate, anterior cingulate cortex, thalamus and regions of prefrontal cortex (PFC) including the orbitofrontal cortex (OFC), dorsolateral PFC (DLPFC), ventromedial PFC (VMPFC) and ventrolateral PFC (VLPFC). Modulating activity within regions of the cortico-striato-thalamo-cortical system may be a common therapeutic mechanism across treatments. We identify future needs and current knowledge gaps that can be mitigated by implementing integrative methods. Future studies should incorporate a systematic, analytical approach to testing objective correlates of treatment response to better understand neurophysiological mechanisms of dysfunction.
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Spindler, Lennart R. B., Andrea I. Luppi, Ram M. Adapa, Michael M. Craig, Peter Coppola, Alexander R. D. Peattie, Anne E. Manktelow, et al. "Dopaminergic brainstem disconnection is common to pharmacological and pathological consciousness perturbation." Proceedings of the National Academy of Sciences 118, no. 30 (July 23, 2021): e2026289118. http://dx.doi.org/10.1073/pnas.2026289118.
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Clinical research into consciousness has long focused on cortical macroscopic networks and their disruption in pathological or pharmacological consciousness perturbation. Despite demonstrating diagnostic utility in disorders of consciousness (DoC) and monitoring anesthetic depth, these cortico-centric approaches have been unable to characterize which neurochemical systems may underpin consciousness alterations. Instead, preclinical experiments have long implicated the dopaminergic ventral tegmental area (VTA) in the brainstem. Despite dopaminergic agonist efficacy in DoC patients equally pointing to dopamine, the VTA has not been studied in human perturbed consciousness. To bridge this translational gap between preclinical subcortical and clinical cortico-centric perspectives, we assessed functional connectivity changes of a histologically characterized VTA using functional MRI recordings of pharmacologically (propofol sedation) and pathologically perturbed consciousness (DoC patients). Both cohorts demonstrated VTA disconnection from the precuneus and posterior cingulate (PCu/PCC), a main default mode network node widely implicated in consciousness. Strikingly, the stronger VTA–PCu/PCC connectivity was, the more the PCu/PCC functional connectome resembled its awake configuration, suggesting a possible neuromodulatory relationship. VTA-PCu/PCC connectivity increased toward healthy control levels only in DoC patients who behaviorally improved at follow-up assessment. To test whether VTA–PCu/PCC connectivity can be affected by a dopaminergic agonist, we demonstrated in a separate set of traumatic brain injury patients without DoC that methylphenidate significantly increased this connectivity. Together, our results characterize an in vivo dopaminergic connectivity deficit common to reversible and chronic consciousness perturbation. This noninvasive assessment of the dopaminergic system bridges preclinical and clinical work, associating dopaminergic VTA function with macroscopic network alterations, thereby elucidating a critical aspect of brainstem–cortical interplay for consciousness.
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Arya, Ashwani, and Gulshan Sindhwani. "A REVIEW ON THE NEURAL CIRCUITS IN ANXIETY DISORDERS." Asian Journal of Pharmaceutical and Clinical Research 9, no. 9 (December 1, 2016): 26. http://dx.doi.org/10.22159/ajpcr.2016.v9s3.11820.
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ABSTRACTAnxiety disorders are among the most common mental, emotional, and behavioral problems. These affect one-eighth of the total population worldwide.Anxiety disorders are a group of mental disorders characterized by irritability, fear, insomnia, nervousness, tachycardia, inability to concentrate,poor coping skills, palpitation, sweating, agoraphobia, and social withdrawal. Brain regions and networks involved in anxiety symptomatology isan effort to better understand the mechanism involved and to develop more effective treatments for the anxiety disorders. Thus, neuroanatomicaland neuroimaging research in anxiety disorders has centered on the role of the amygdala, reciprocal connections between the amygdala and theprefrontal cortex, and, most recently, alterations in interoceptive processing by the anterior insula. Anxiety disorders are characterized by alterationsin a diverse range of neurochemical systems, suggesting ample novel targets for drug therapies. The neurotransmitter like corticotropin-releasingfactor, neuropeptides (substance P, neuropeptide Y, oxytocin, orexin, and galanin) are implicated in anxiety pathways. Each of these active areas ofresearch holds promise for expanding and improving evidence-based treatment options for individuals suffering with clinical anxiety. Therefore,this article gives the information on the neurocognitive mechanisms, causes, neurotransmitter involved in anxiety disorders and emphasize on thetherapeutic targets for anxiety disorders.Keywords: Anxiety, Stress, Amygdala, Corticotropin releasing factor, Insula, Thalamus.
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Zelena, Dora, Ophelie Menant, Frederic Andersson, and Elodie Chaillou. "Periaqueductal gray and emotions: the complexity of the problem and the light at the end of the tunnel, the magnetic resonance imaging." Endocrine Regulations 52, no. 4 (October 1, 2018): 222–38. http://dx.doi.org/10.2478/enr-2018-0027.
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AbstractThe periaqueductal gray (PAG) is less referred in relationship with emotions than other parts of the brain (e.g. cortex, thalamus, amygdala), most probably because of the difficulty to reach and manipulate this small and deeply lying structure. After defining how to evaluate emotions, we have reviewed the literature and summarized data of the PAG contribution to the feeling of emotions focusing on the behavioral and neurochemical considerations. In humans, emotions can be characterized by three main domains: the physiological changes, the communicative expressions, and the subjective experiences. In animals, the physiological changes can mainly be studied. Indeed, early studies have considered the PAG as an important center of the emotions-related autonomic and motoric processes. However, in vivo imaging have changed our view by highlighting the PAG as a significant player in emotions-related cognitive processes. The PAG lies on the crossroad of networks important in the regulation of emotions and therefore it should not be neglected. In vivo imaging represents a good tool for studying this structure in living organism and may reveal new information about its role beyond its importance in the neurovegetative regulation.
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Karsan, Nazia. "Pathophysiology of Migraine." CONTINUUM: Lifelong Learning in Neurology 30, no. 2 (April 2024): 325–43. http://dx.doi.org/10.1212/con.0000000000001412.
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ABSTRACT Objective This article provides an overview of the current understanding of migraine pathophysiology through insights gained from the extended symptom spectrum of migraine, neuroanatomy, migraine neurochemistry, and therapeutics. Latest Developments Recent advances in human migraine research, including human experimental migraine models and functional neuroimaging, have provided novel insights into migraine attack initiation, neurochemistry, neuroanatomy, and therapeutic substrates. It has become clear that migraine is a neural disorder, in which a wide range of brain areas and neurochemical systems are implicated, producing a heterogeneous clinical phenotype. Many of these neural pathways are monoaminergic and peptidergic, such as those involving calcitonin gene-related peptide and pituitary adenylate cyclase-activating polypeptide. We are currently witnessing an exciting era in which specific drugs targeting these pathways have shown promise in treating migraine, including some studies suggesting efficacy before headache has even started. Essential Points Migraine is a brain disorder involving both headache and altered sensory, limbic, and homeostatic processing. A complex interplay between neurotransmitter systems, physiologic systems, and pain processing likely occurs. Targeting various therapeutic substrates within these networks provides an exciting avenue for future migraine therapeutics.
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Krejčí, Milada, and Dobroslava Jandová. "Homeostasis and balance in senium." Acta Salus Vitae 8, no. 2 (December 8, 2020): 14–27. http://dx.doi.org/10.58743/asv2020vol8no2.240.
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The body's homeostasis ensures the individual's survival in a constantly changing environment, such as changes and fluctuations of temperature, humidity, pressure, etc. The central nervous system and cardiovascular system play a priority in maintaining homeostasis. State of balance is closely related to the theory of homeostasis and homedynamics, where the term homeostasis is characterized as the tendency of the organism to a relatively stable balance between interdependent elements maintained by physiological processes. The study is aimed on content and descriptive analysis of the context of homeostasis, homeodynamics and bio-psycho-social balance in aging in frame of the GAČR project ID 17-25710S “Basic research of balance changes in seniors”. Methods of content and descriptive analysis were used as a base. There is experimental evidence that various forms of stress, especially when severe or recurrent, can induce corresponding structural and neurochemical or neurophysiological changes in the neural and glial networks. It can be assumed that many of these stress-induced structural and functional changes in the CNS may cause the development of some neuropsychiatric disorders typical of old age. According to yoga practice, it is known that many of these changes are reversible with sufficient recovery time.
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Regala, Joana, Camila Nóbrega, and João Reis. "423 - Visual Hallucinations in Parkinson Disease and Dementia with Lewy Bodies: a review." International Psychogeriatrics 32, S1 (October 2020): 139. http://dx.doi.org/10.1017/s1041610220002768.
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Visual Hallucinations (VH) are a common psychiatric symptom of Parkinson’s Disease (PD) and Dementia with Lewy Bodies (DLB). According to the Perception-Attention Deficits Model, VH stem from impaired perceptual (bottom-up), including dorsal (DVS) and ventral visual streams (VVS), and attentional (top-down) processes, with a persistent Default Mode Network (DMN) activity and a dysfunctional imbalance of Dorsal (DAN) and Ventral Attentional Networks (VAN).We review the literature on the neurobiological underpinnings of VH in DLB and PD, concerning overlapping and different mechanisms.In DLB hallucinators, PET-scan findings of disconnection between higher and primary visual areas and dysfunctional recruitment of the VVS, corroborate other imaging and neuropathologic studies which document inferior longitudinal fasciculus damage and increased temporal lobe Lewy body (LB) pathology. The alteration of network topography is more pronounced in the DAN and DMN. The involvement of anterior cortical regions, clustering around attentional networks, is demonstrated in neuropathologic, volumetric and perfusion studies. VH severity closely correlates with anterior cingulate cortex and inferior temporal cortex hypoperfusion, structural changes in the DVS (superior parietal gyrus and precuneus) and increased diffusivity of the right thalamic projections to parieto-occipital cortices. Thalamocortical dysfunction alongside decreased cholinergic activity in reticular nucleus, which receive projections from the nucleus basalis of Meynert, seems to play a crucial role.Both DLB and demented PD hallucinators have more frontal cortical atrophy, yet greater in DLB, supporting top-down mechanisms.Regarding PD hallucinators, findings of cortical atrophy in inferior parietal lobule, cuneus, lingual lobule, and precentral gyrus correlated with hallucination scores. However, some studies did not evidence volumetric cortical differences between hallucinators and non-hallucinators. Moreover, LB are not necessarily present in hallucinators, suggesting other neuropathologic mechanisms in the genesis of VH, namely altered neurochemical circuitry. Volume loss in pedunculopontine nucleus and right-thalamus support the hypothesis of a dysfunctional cholinergic brainstem control of the cortex. PET-scan studies discovered higher 5-HT2A receptor levels in the inferolateral temporal and prefrontal cortices. A greater nigrostriatal impairment is documented in the right-caudate of hallucinators. Therefore, VH may arise from an inability to activate DAN (in which caudate is involved) and consequent faulty visuo-perceptual processing by DMN and VAN.
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Lanza, Giuseppe, Placido Bramanti, Mariagiovanna Cantone, Manuela Pennisi, Giovanni Pennisi, and Rita Bella. "Vascular Cognitive Impairment through the Looking Glass of Transcranial Magnetic Stimulation." Behavioural Neurology 2017 (2017): 1–16. http://dx.doi.org/10.1155/2017/1421326.
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In the last years, there has been a significant growth in the literature exploiting transcranial magnetic stimulation (TMS) with the aim at gaining further insights into the electrophysiological and neurochemical basis underlying vascular cognitive impairment (VCI). Overall, TMS points at enhanced brain cortical excitability and synaptic plasticity in VCI, especially in patients with overt dementia, and neurophysiological changes seem to correlate with disease process and progress. These findings have been interpreted as part of a glutamate-mediated compensatory effect in response to vascular lesions. Although a single TMS parameter owns low specificity, a panel of measures can support the VCI diagnosis, predict progression, and possibly identify early markers of “brain at risk” for future dementia, thus making VCI a potentially preventable cause of both vascular and degenerative dementia in late life. Moreover, TMS can be also exploited to select and evaluate the responders to specific drugs, as well as to become an innovative rehabilitative tool in the attempt to restore impaired neural plasticity. The present review provides a perspective of the different TMS techniques by further understanding the cortical electrophysiology and the role of distinctive neurotransmission pathways and networks involved in the pathogenesis and pathophysiology of VCI and its subtypes.
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He, Shao-Qiu, Chi Zhang, Xue-Wei Wang, Qian Huang, Jing Liu, Qing Lin, Hua He, Da-Zhi Yang, Scheffer C. Tseng, and Yun Guan. "HC-HA/PTX3 from Human Amniotic Membrane Induced Differential Gene Expressions in DRG Neurons: Insights into the Modulation of Pain." Cells 13, no. 22 (November 15, 2024): 1887. http://dx.doi.org/10.3390/cells13221887.
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Background: The biologics derived from human amniotic membranes (AMs) demonstrate potential pain-inhibitory effects in clinical settings. However, the molecular basis underlying this therapeutic effect remains elusive. HC-HA/PTX3 is a unique water-soluble regenerative matrix that is purified from human AMs. We examined whether HC-HA/PTX3 can modulate the gene networks and transcriptional signatures in the dorsal root ganglia (DRG) neurons transmitting peripheral sensory inputs to the spinal cord. Methods: We conducted bulk RNA-sequencing (RNA-seq) of mouse DRG neurons after treating them with HC-HA/PTX3 (15 µg/mL) for 10 min and 24 h in culture. Differential gene expression analysis was performed using the limma package, and Gene Ontology (GO) and protein–protein interaction (PPI) analyses were conducted to identify the networks of pain-related genes. Western blotting and in vitro calcium imaging were used to examine the protein levels and signaling of pro-opiomelanocortin (POMC) in DRG neurons. Results: Compared to the vehicle-treated group, 24 h treatment with HC-HA/PTX3 induced 2047 differentially expressed genes (DEGs), which were centered on the ATPase activity, receptor–ligand activity, and extracellular matrix pathways. Importantly, PPI analysis revealed that over 50 of these DEGs are closely related to pain and analgesia. Notably, HC-HA/PTX3 increased the expression and signaling pathway of POMC, which may affect opioid analgesia. Conclusions: HC-HA/PTX3 induced profound changes in the gene expression in DRG neurons, centered around various neurochemical mechanisms associated with pain modulation. Our findings suggest that HC-HA/PTX3 may be an important biological active component in human AMs that partly underlies its pain inhibitory effect, presenting a new strategy for pain treatment.
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Beyene, Abraham G. "(Invited) Unraveling Somatodendritic Dopamine Release Using Dopafilm, a Two-Dimensional Chemi-Sensitive Substrate for Real-Time Measurement of Neurochemical Efflux." ECS Meeting Abstracts MA2022-01, no. 8 (July 7, 2022): 700. http://dx.doi.org/10.1149/ma2022-018700mtgabs.
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Neurons communicate through chemical signaling molecules that may diffuse beyond their point of release in axon terminals and modulate the activity of larger neuronal networks in a process known as volume transmission. Molecules such as dopamine belong to this class of diffusive neurotransmitters. In addition to canonical release from axonal arbors, somatodendritic dopamine release constitutes an important signaling mechanism for dopamine neurons. However, the spatiotemporal dynamics as well as regulatory mechanisms of somatodendritic release have not been adequately explored, and it is not clear if release arises from soma or dendrites. These gaps in our understanding of somatodendritic dopamine efflux are driven in large part by the inability of current assays to measure neurochemical effluxes at requisite spatial and temporal scales. To address this, we developed DopaFilm, a 2-dimensional chemi-sensitive surface on which primary dopamine neuron cultures can be grown. DopaFilm is developed by drop-casting a solution of single strand DNA functionalized single wall carbon nanotube-based catecholamine sensors (NIRcat) onto glass substrates and passivating the surfaces with poly-lysine. DopaFilm enabled recording of dopamine efflux with exquisite sub-cellular resolution and millisecond temporal resolution. When deployed in perikaryal of dopamine neurons, DopaFilm reveals that somatodendritic effluxes of dopamine primary arise from dendrites and not from the soma. Coupled with immunofluorescence and super resolution imaging, our work affords explorations of the regulatory mechanism of dendritic dopamine release, as well as shed light on the spatiotemporal dynamics and heterogeneities associated with dendritic release.
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Gerasimenko, Yury, Chet Preston, Hui Zhong, Roland R. Roy, V. Reggie Edgerton, and Prithvi K. Shah. "Rostral lumbar segments are the key controllers of hindlimb locomotor rhythmicity in the adult spinal rat." Journal of Neurophysiology 122, no. 2 (August 1, 2019): 585–600. http://dx.doi.org/10.1152/jn.00810.2018.
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The precise location and functional organization of the spinal neuronal locomotor-related networks in adult mammals remain unclear. Our recent neurophysiological findings provided empirical evidence that the rostral lumbar spinal cord segments play a critical role in the initiation and generation of the rhythmic activation patterns necessary for hindlimb locomotion in adult spinal rats. Since added epidural stimulation at the S1 segments significantly enhanced the motor output generated by L2 stimulation, these data also suggested that the sacral spinal cord provides a strong facilitory influence in rhythm initiation and generation. However, whether L2 will initiate hindlimb locomotion in the absence of S1 segments, and whether S1 segments can facilitate locomotion in the absence of L2 segments remain unknown. Herein, adult rats received complete spinal cord transections at T8 and then at either L2 or S1. Rats with spinal cord transections at T8 and S1 remained capable of generating coordinated hindlimb locomotion when receiving epidural stimulation at L2 and when ensembles of locomotor related loadbearing input were present. In contrast, minimal locomotion was observed when S1 stimulation was delivered after spinal cord transections at T8 and L2. Results were similar when the nonspecific serotonergic agonists were administered. These results demonstrate in adult rats that rostral lumbar segments are essential for the regulation of hindlimb locomotor rhythmicity. In addition, the more caudal spinal networks alone cannot control locomotion in the absence of the rostral segments around L2 even when loadbearing rhythmic proprioceptive afferent input is imposed. NEW & NOTEWORTHY The exact location of the spinal neuronal locomotor-related networks in adult mammals remains unknown. The present data demonstrate that when the rostral lumbar spinal segments (~L2) are completely eliminated in thoracic spinal adult rats, hindlimb stepping is not possible with neurochemical modulation of the lumbosacral cord. In contrast, eliminating the sacral cord retains stepping ability. These observations highlight the importance of rostral lumbar segments in generating effective mammalian locomotion.
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Schmitt, Oliver, Christian Nitzsche, Peter Eipert, Vishnu Prathapan, Marc-Thorsten Hütt, and Claus Hilgetag. "Reaction-diffusion models in weighted and directed connectomes." PLOS Computational Biology 18, no. 10 (October 28, 2022): e1010507. http://dx.doi.org/10.1371/journal.pcbi.1010507.
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Connectomes represent comprehensive descriptions of neural connections in a nervous system to better understand and model central brain function and peripheral processing of afferent and efferent neural signals. Connectomes can be considered as a distinctive and necessary structural component alongside glial, vascular, neurochemical, and metabolic networks of the nervous systems of higher organisms that are required for the control of body functions and interaction with the environment. They are carriers of functional epiphenomena such as planning behavior and cognition, which are based on the processing of highly dynamic neural signaling patterns. In this study, we examine more detailed connectomes with edge weighting and orientation properties, in which reciprocal neuronal connections are also considered. Diffusion processes are a further necessary condition for generating dynamic bioelectric patterns in connectomes. Based on our high-precision connectome data, we investigate different diffusion-reaction models to study the propagation of dynamic concentration patterns in control and lesioned connectomes. Therefore, differential equations for modeling diffusion were combined with well-known reaction terms to allow the use of connection weights, connectivity orientation and spatial distances. Three reaction-diffusion systems Gray-Scott, Gierer-Meinhardt and Mimura-Murray were investigated. For this purpose, implicit solvers were implemented in a numerically stable reaction-diffusion system within the framework of neuroVIISAS. The implemented reaction-diffusion systems were applied to a subconnectome which shapes the mechanosensitive pathway that is strongly affected in the multiple sclerosis demyelination disease. It was found that demyelination modeling by connectivity weight modulation changes the oscillations of the target region, i.e. the primary somatosensory cortex, of the mechanosensitive pathway. In conclusion, a new application of reaction-diffusion systems to weighted and directed connectomes has been realized. Because the implementation were performed in the neuroVIISAS framework many possibilities for the study of dynamic reaction-diffusion processes in empirical connectomes as well as specific randomized network models are available now.
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Mason, Sarah L., Miriam Schaepers, and Roger A. Barker. "Problems with Social Cognition and Decision-Making in Huntington’s Disease: Why Is it Important?" Brain Sciences 11, no. 7 (June 24, 2021): 838. http://dx.doi.org/10.3390/brainsci11070838.
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Huntington’s disease starts slowly and progresses over a 15–20 year period. Motor changes begin subtly, often going unnoticed by patients although they are typically visible to those close to them. At this point, it is the early non-motor problems of HD that arguably cause the most functional impairment. Approximately 65% of gene carriers will experience a reduction in their occupational level, and just under half will feel unable to manage their finances independently before a clinical diagnosis is made. Understanding what drives this impairment in activities of daily living is the key to helping people with HD to live more independently for longer, especially in early disease. Early cognitive decline is likely to play a contributory factor although few studies have looked directly at this relationship. Recently, it has been shown that along with the well documented dysexecutive syndrome seen in HD, changes in social cognition and decision-making are more common than previously thought. Furthermore, some of the early neuropathological and neurochemical changes seen in HD disrupt networks known to be involved in social functioning. In this review, we explore how HD changes the way individuals interact in a social world. Specifically, we summarise the literature on both classical and social decision-making (value-based decision-making in a social context) along with studies of theory of mind, empathy, alexithymia, and emotion recognition in HD. The literature specific to HD is discussed and supported by evidence from similar neurodegenerative disorders and healthy individuals to propose future directions and potential therapeutic avenues to be explored.
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Rasch, Björn, and Jan Born. "About Sleep's Role in Memory." Physiological Reviews 93, no. 2 (April 2013): 681–766. http://dx.doi.org/10.1152/physrev.00032.2012.
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Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of “sleep and memory” research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.
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Drouin, Candice, Michelle Page, and Barry Waterhouse. "Methylphenidate Enhances Noradrenergic Transmission and Suppresses Mid- and Long-Latency Sensory Responses in the Primary Somatosensory Cortex of Awake Rats." Journal of Neurophysiology 96, no. 2 (August 2006): 622–32. http://dx.doi.org/10.1152/jn.01310.2005.
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Noradrenergic neurons send widespread projections to sensory networks throughout the brain and regulate sensory processing via norepinephrine (NE) release. As a catecholamine reuptake blocker, methylphenidate (MPH) is likely to interact with noradrenergic transmission and NE modulatory action on sensory systems. To characterize the neurochemical actions of MPH in the primary sensory cortex of freely behaving rats and their consequences on sensory processing, we measured extracellular NE levels in the primary somatosensory (SI) cortex by microdialysis and recorded basal and sensory-evoked discharge of infragranular SI cortical neurons, before and after intraperitoneal administrations of saline or MPH (1 and 5 mg/kg). Both doses of MPH significantly increased NE levels in the SI cortex (+64 and +101%, respectively). In most neurons, stimulation of the whisker-pad induced a triphasic response, consisting of a short-latency excitation [4.7 ± 0.2 (SE) ms] followed by a postexcitatory inhibition (36 ± 1.5 ms) and a long-latency excitation (105 ± 2.6 ms). Under control conditions, the behavioral state of the animal was correlated with the magnitude of the short-latency excitation but not with other aspects of the basal and sensory-evoked discharge of SI cortical neurons. At 5 mg/kg, MPH significantly increased locomotor activity and induced a significant suppression of the short-latency excitation, which probably resulted from the MPH-induced change in behavior. In addition, both doses of MPH suppressed the postexcitatory inhibition and the long-latency excitation evoked by the stimulation of the whisker pad. These effects did not seem to result from the locomotor effect of MPH and probably involved MPH-induced enhancement of noradrenergic transmission.
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Santana, Noemí, Guadalupe Mengod, and Francesc Artigas. "Expression of α1-adrenergic receptors in rat prefrontal cortex: cellular co-localization with 5-HT2A receptors." International Journal of Neuropsychopharmacology 16, no. 5 (June 1, 2013): 1139–51. http://dx.doi.org/10.1017/s1461145712001083.
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Abstract The prefrontal cortex (PFC) is involved in behavioural control and cognitive processes that are altered in schizophrenia. The brainstem monoaminergic systems control PFC function, yet the cells/networks involved are not fully known. Serotonin (5-HT) and norepinephrine (NE) increase PFC neuronal activity through the activation of α1-adrenergic receptors (α1ARs) and 5-HT2A receptors (5-HT2ARs), respectively. Neurochemical and behavioural interactions between these receptors have been reported. Further, classical and atypical antipsychotic drugs share nmin vitro affinity for α1ARs while having preferential affinity for D2 and 5-HT2ARs, respectively. Using double in situ hybridization we examined the cellular expression of α1ARs in pyramidal (vGluT1-positive) and GABAergic (GAD65/67-positive) neurons in rat PFC and their co-localization with 5-HT2ARs. α1ARs are expressed by a high proportion of pyramidal (59–85%) and GABAergic (52–79%) neurons. The expression in pyramidal neurons exhibited a dorsoventral gradient, with a lower percentage of α1AR-positive neurons in infralimbic cortex compared to anterior cingulate and prelimbic cortex. The expression of α1A, α1B and α1D adrenergic receptors was segregated in different layers and subdivisions. In all them there is a high co-expression with 5-HT2ARs (∼80%). These observations indicate that NE controls the activity of most PFC pyramidal neurons via α1ARs, either directly or indirectly, via GABAergic interneurons. Antipsychotic drugs can thus modulate the activity of PFC via α1AR blockade. The high co-expression with 5-HT2ARs indicates a convergence of excitatory serotonergic and noradrenergic inputs onto the same neuronal populations. Moreover, atypical antipsychotics may exert a more powerful control of PFC function through the simultaneous blockade of α1ARs and 5-HT2ARs.
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Chen, Yongjun, Ziyu Meng, Zongfeng Zhang, Yajing Zhu, Rui Gao, Xuan Cao, Ling Tan, et al. "The right thalamic glutamate level correlates with functional connectivity with right dorsal anterior cingulate cortex/middle occipital gyrus in unmedicated obsessive–compulsive disorder: A combined fMRI and 1H-MRS study." Australian & New Zealand Journal of Psychiatry 53, no. 3 (October 24, 2018): 207–18. http://dx.doi.org/10.1177/0004867418806370.
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Objective: The imbalance in neurotransmitter and neuronal metabolite concentration within cortico-striato-thalamo-cortical (CSTC) circuit contributes to obsessive–compulsive disorder’s (OCD) onset. Previous studies showed that glutamate mediated upregulation of resting-state activity in healthy people. However, there have been few studies investigating the correlational features between functional and neurochemical alterations in OCD. Methods: We utilize a combined resting-state functional magnetic resonance imaging (rs-fMRI) and proton magnetic resonance spectroscopy (1H-MRS) approach to investigate the altered functional connectivity (FC) in association with glutamatergic dysfunction in OCD pathophysiology. Three regions of interest are investigated, i.e., medial prefrontal cortex and bilateral thalamus, for seed-based whole-brain FC analysis as well as MRS data acquisition. There are 23 unmedicated adult OCD patients and 23 healthy controls recruited for brain FC analysis. Among them, 12 OCD and 8 controls are performed MRS data acquisition. Results: Besides abnormal FC within CSTC circuit, we also find altered FCs in large-scale networks outside CSTC circuit, including occipital area and limbic and motor systems. The decreased FC between right thalamus and right middle occipital gyrus (MOG) is correlated with glutamatergic signal within right thalamus in OCD patients. Moreover, the FC between right thalamus and right dorsal anterior cingulate cortex (dACC) is associated with glutamate level in right thalamus, specifically in patient’s group. Finally, the FC between right thalamus and right MOG is correlated with patient’s Yale–Brown Obsessive Compulsive Scale (YBOCS) compulsion and total scores, while the right thalamic glutamatergic signal is associated with YBOCS-compulsion score. Conclusion: Our findings showed that the coupled intrinsic functional–biochemical alterations existed both within CSTC circuit and from CSTC to occipital lobe in OCD pathophysiology.
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Ziegler, Christiane, Annette Harsch, and Wolfgang Göpel. "Natural neural networks for quantitative sensing of neurochemicals: an artificial neural network analysis." Sensors and Actuators B: Chemical 65, no. 1-3 (June 2000): 160–62. http://dx.doi.org/10.1016/s0925-4005(99)00343-3.
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Oleskin, Alexander V., and Vladimir S. Kurdyumov. "Cellular Paradigm of Network Organization: Implications for Present-Day Society." Economic Strategies 144 (October 23, 2020): 68–77. http://dx.doi.org/10.33917/es-6.172.2020.68-77.
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Microorganisms and cultivated cells from human or animal tissues form complex network structures (colonies, biofilms, flocs, granules, etc.) that are characterized by efficient communication and behavior coordination in the absence of a central pacemaker. The decentralized (flat) network organization of such structures is due to the functioning of (a) information-transmitting intercellular contacts, (b) a signal field created by distant communication systems, including the quorum-sensing system; and (c) a biopolymer matrix that cements the cells of the whole network structure. Microbial network structures exist in the human organism, especially in the gastro-intestinal (GI) tract. The cellular networks engage in complex interaction with the host organism. The organism represents a complex combination of hierarchical structures and decentralized networks and includes the brain, the peripheral nervous system, the immune system, and the endocrine system. The interaction between the microbiota and the host may produce both positive and negative effects on the host’s physical and mental health, because decentralized networks are known to possess not only useful but also potentially harmful properties. Communication between microbial cells and the host organism involves neurochemicals, i.e., chemical compounds, whose functions include impulse transmission between nervous cells. In the final section, the cellular paradigm of network organization is envisaged as the conceptual basis of organizational technology aimed at creating efficient non-hierarchical creative teams that are cemented by common values and goals (the network matrix).
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Hobson, J. A., R. Lydic, and H. A. Baghdoyan. "Evolving concepts of sleep cycle generation: From brain centers to neuronal populations." Behavioral and Brain Sciences 9, no. 3 (September 1986): 371–400. http://dx.doi.org/10.1017/s0140525x00046215.
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AbstractAs neurophysiological investigations of sleep cycle control have provided an increasingly detailed picture of events at the cellular level, the concept that the sleep cycle is generated by the interaction of multiple, anatomically distributed sets of neurons has gradually replaced the hypothesis that sleep is generated by a single, highly localized neuronal oscillator.Cell groups that discharge during rapid-eye-movement (REM) sleep (REM-on) and neurons that slow or cease firing during REM sleep (REM-off) have long been thought to comprise at least two neurochemically distinct populations. The fact that putatively cholinoceptive and/or cholinergic (REM-on) and putatively aminergic (REM-off) cell populations discharge reciprocally over the sleep cycle suggests a causal interdependence.In some brain stem areas these cell groups are not anatomically segregated and may instead be neurochemically mixed (interpenetrated). This finding raises important theoretical and practical issues not anticipated in the original reciprocal-interaction model. The electrophysiological evidence concerning the REM-on and REM-off cell groups suggests a gradient of sleep-dependent membrane excitability changes that may be a function of the connectivity strength within an anatomically distributed neuronal network. The connectivity strength may be influenced by the degree of neurochemical interpenetration between the REM-on and REM-offcells. Recognition of these complexities forces us to revise the reciprocal-interaction model and to seek new methods to test its tenets.Cholinergic microinjection experiments indicate that some populations of REM-on cells can execute specific portions of the REM sleep syndrome or block the generation of REM sleep. This observation suggests that the order of activation within the anatomically distributed generator populations may be critical in determining behavioral outcome. Support for the cholinergic tenets of the reciprocal-interaction model has been reinforced by observations from sleep-disorders medicine.Specific predictions of the reciprocal-interaction model and suggestions for testing these predictions are enumerated for future experimental programs that aim to understand the cellular and molecular basis of the mammalian sleep cycle.
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Miller, Justin Robert, Suzanne Neumueller, Clarissa Muere, Samantha Olesiak, Lawrence Pan, Matthew R. Hodges, and Hubert V. Forster. "Changes in neurochemicals within the ventrolateral medullary respiratory column in awake goats after carotid body denervation." Journal of Applied Physiology 115, no. 7 (October 1, 2013): 1088–98. http://dx.doi.org/10.1152/japplphysiol.00293.2013.
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A current and major unanswered question is why the highly sensitive central CO2/H+ chemoreceptors do not prevent hypoventilation-induced hypercapnia following carotid body denervation (CBD). Because perturbations involving the carotid bodies affect central neuromodulator and/or neurotransmitter levels within the respiratory network, we tested the hypothesis that after CBD there is an increase in inhibitory and/or a decrease in excitatory neurochemicals within the ventrolateral medullary column (VMC) in awake goats. Microtubules for chronic use were implanted bilaterally in the VMC within or near the pre-Bötzinger Complex (preBötC) through which mock cerebrospinal fluid (mCSF) was dialyzed. Effluent mCSF was collected and analyzed for neurochemical content. The goats hypoventilated (peak +22.3 ± 3.4 mmHg PaCO2) and exhibited a reduced CO2 chemoreflex (nadir, 34.8 ± 7.4% of control ΔV̇E/ΔPaCO2) after CBD with significant but limited recovery over 30 days post-CBD. After CBD, GABA and glycine were above pre-CBD levels (266 ± 29% and 189 ± 25% of pre-CBD; P < 0.05), and glutamine and dopamine were significantly below pre-CBD levels ( P < 0.05). Serotonin, substance P, and epinephrine were variable but not significantly ( P > 0.05) different from control after CBD. Analyses of brainstem tissues collected 30 days after CBD exhibited 1) a midline raphe-specific reduction ( P < 0.05) in the percentage of tryptophan hydroxylase–expressing neurons, and 2) a reduction ( P < 0.05) in serotonin transporter density in five medullary respiratory nuclei. We conclude that after CBD, an increase in inhibitory neurotransmitters and a decrease in excitatory neuromodulation within the VMC/preBötC likely contribute to the hypoventilation and attenuated ventilatory CO2 chemoreflex.
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Parent, Jourdan H., Kaitlin Cassady, William J. Jagust, and Anne S. Berry. "Pathological and neurochemical correlates of locus coeruleus functional network activity." Biological Psychology 192 (October 2024): 108847. http://dx.doi.org/10.1016/j.biopsycho.2024.108847.
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Chernock, Michelle L., David T. Larue, and Jeffery A. Winer. "A periodic network of neurochemical modules in the inferior colliculus." Hearing Research 188, no. 1-2 (February 2004): 12–20. http://dx.doi.org/10.1016/s0378-5955(03)00340-x.
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Xu, Meng, Yuewu Zhao, Guanghui Xu, Yuehu Zhang, Shengkai Sun, Yan Sun, Jine Wang, and Renjun Pei. "Recent Development of Neural Microelectrodes with Dual-Mode Detection." Biosensors 13, no. 1 (December 30, 2022): 59. http://dx.doi.org/10.3390/bios13010059.
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Neurons communicate through complex chemical and electrophysiological signal patterns to develop a tight information network. A physiological or pathological event cannot be explained by signal communication mode. Therefore, dual-mode electrodes can simultaneously monitor the chemical and electrophysiological signals in the brain. They have been invented as an essential tool for brain science research and brain-computer interface (BCI) to obtain more important information and capture the characteristics of the neural network. Electrochemical sensors are the most popular methods for monitoring neurochemical levels in vivo. They are combined with neural microelectrodes to record neural electrical activity. They simultaneously detect the neurochemical and electrical activity of neurons in vivo using high spatial and temporal resolutions. This paper systematically reviews the latest development of neural microelectrodes depending on electrode materials for simultaneous in vivo electrochemical sensing and electrophysiological signal recording. This includes carbon-based microelectrodes, silicon-based microelectrode arrays (MEAs), and ceramic-based MEAs, focusing on the latest progress since 2018. In addition, the structure and interface design of various types of neural microelectrodes have been comprehensively described and compared. This could be the key to simultaneously detecting electrochemical and electrophysiological signals.
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Praveen Kumar Yadav and Kumud Sahu. "Review article: Neural networks in psychiatry." World Journal of Advanced Research and Reviews 17, no. 1 (January 30, 2023): 343–52. http://dx.doi.org/10.30574/wjarr.2023.17.1.0018.
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Mental health is an intricate branch of medicine that involve the various brain circuits including frontal, temporal and occipital lobes, may also involve the structure and functional unit of brain. Many psychiatrist treat on the basis of subjective experience rather than implying the pathophysiology of the disease process. So in this article, we highlighted the concept of various brain circuits, role of neurochemicals and its involvement in various neuro-psychiatric illness like schizophrenia, Obsessive compulsive disorder, depression etc. Analogous to our human brain is Deep Neural Network (DNN) and Machine learning, based on "Graph Theory"(Artificial Neural Network), play a crucial role in working of Artificial Intelligence (AI) techniques. Various neuroimaging techniques like fMRI, is described in detail. Importance of AI in early diagnosis, individual treatment, counselling and research of various illness and AI based applications has been narrated.
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Bulumulla, Chandima, Andrew T. Krasley, and Abraham G. Beyene. "Carbon Nanotube Sensors Enable Visualization of Dopamine Neuromodulation at the Resolution of a Single Chemical Synapse." ECS Meeting Abstracts MA2023-01, no. 9 (August 28, 2023): 1120. http://dx.doi.org/10.1149/ma2023-0191120mtgabs.
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Among the organs in our body, the brain easily remains the most intriguing in terms of its complexity and function. Nerve cells, which are the functional building blocks of the brain, operate in complex networks that underpin most of the brain’s capabilities, including ability to learn, remember, initiate and orchestrate complex movement. In systems neuroscience, behavioral assays and large-scale neuronal activity recording have broadened our understanding of the role that specific brain regions and neuronal circuits play in a behaving animal. An equally exciting aspect of neuroscience concerns itself with the cellular and molecular underpinnings of nerve cell function. Unique among all the organs, the brain’s constituent cells, neurons, need to communicate with another in intricate networks that are responsible for circuit function, and most of this communication is enabled by chemical cues that are released between neurons. Better understanding of neuronal communication via chemical release from synapses requires technologies that can help us visualize and measure the spatial and temporal dynamics of these chemical signals. Our lab seeks to address this challenge by developing optical biosensors with ultra-low detection capabilities, high spatial resolution and signal-to-noise ratio. To study chemical synapses at high spatial resolution, we use primary dopamine neuron cultures derived from rats and mice as a model system. Dopamine neuron signaling is critical for learning and motor control, and its aberration is implicated in a wide range of neurological and psychiatric disorders. Furthermore, dopamine is a neuromodulator, and it is a neurochemical that is predicted to be highly diffusive in its spatial signaling. Our lab and several others have developed ssDNA functionalized SWCNT optical sensors to study catecholaminergic neurotransmitters, including dopamine. In a recent publication we reported an assay to study dopamine effluxes from primary dopaminergic neurons using a chemi-sensitive 2D substrate (DopaFilm). DopaFilm is fabricated from solution phase SWCNT-sensors in two simple steps: (1) surface functionalization of glass coverslips using silane chemistry to anchor nanosensors (2) drop casting of nanotube sensor solution to create the 2D nanofilm followed by passivation with a thin layer of poly(D-lysine). Primary dopamine neurons plated on DopaFilm are allowed to grow and mature (2 – 6 weeks depending on the experiment). Dopamine release activity can be imaged by recording the NIR emission (900-1400 nm) and at excitation with a 785nm laser. With this technology we were able to faithfully measure dopamine concentrations as low as 1nM with DopaFilm, which has an apparent dissociation constant of 268nM. In 2D cultures, we routinely observed spontaneous and evoked dendritic and axonal DA release events with bouton level spatial resolutions and sub-second temporal resolutions. With signal-to-noise ratios above 50 and comparable on and off-kinetics to latest genetically encoded dopamine sensors (dLight1 and GRABDA), DopaFilm is by far the most sensitive technology to study dopamine chemical signaling with the resolution of a single synapse. The technology allows the study of an entire neuron at the resolution of a single synapse. We combine functional imaging data with pharmacological and genetic perturbations to dissect the role that circuit effects and specific genes (proteins) play in dopamine synthesis, packaging, and release. Additionally, by taking advantage of the NIR emission of SWCNTs, we are able to multiplex dopamine release imaging with Ca2+ activity in orthogonal channels, a feat that is yet to be demonstrated with any competing technology.