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Journal articles on the topic 'Excitatory neurotransmitter'

Author: Grafiati

Published: 5 June 2025

Last updated: 16 July 2025

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1

Kim, Dongshin, and Jang-Sik Lee. "Emulating Excitatory and Inhibitory Functions in Artificial Synaptic Devices." ECS Meeting Abstracts MA2022-02, no. 33 (2022): 2585. http://dx.doi.org/10.1149/ma2022-02332585mtgabs.

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Synaptic signals are controlled by neurotransmitters. The synaptic signals can be excited or inhibited depending on the types of neurotransmitters. The demonstration of the balancing between excitatory and inhibitory signals has important implications for the complex and efficient computing of the nervous system. Emulating the excitatory-inhibitory balancing behaviors of the nervous system is one way to establish neuromorphic computing. In this study, we demonstrate artificial synapses using PEDOT:PSS channel and neurotransmitter solutions to emulate the excitatory-inhibitory balancing behavio

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Huang, Chun-Ping, Yi-Wen Lin, Der-Yen Lee, and Ching-Liang Hsieh. "Electroacupuncture Relieves CCI-Induced Neuropathic Pain Involving Excitatory and Inhibitory Neurotransmitters." Evidence-Based Complementary and Alternative Medicine 2019 (October 20, 2019): 1–9. http://dx.doi.org/10.1155/2019/6784735.

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Neuropathic pain caused by peripheral tissue injuries to the higher brain regions still has no satisfactory therapy. Disruption of the balance of excitatory and inhibitory neurotransmitters is one of the underlying mechanisms that results in chronic neuropathic pain. Targeting neurotransmitters and related receptors may constitute a novel approach for treating neuropathic pain. We investigated the effects of electroacupuncture (EA) on chronic constriction injury- (CCI-) induced neuropathic pain. The mechanical allodynia and thermal hyperalgesia pain behaviors were relieved by 15 Hz EA but not

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Stahl, Stephen M. "Glutamate: The Universal Excitatory Neurotransmitter." Psychiatric Annals 27, no. 3 (1997): 152–55. http://dx.doi.org/10.3928/0048-5713-19970301-03.

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Herring, B. E., K. Silm, R. H. Edwards, and R. A. Nicoll. "Is Aspartate an Excitatory Neurotransmitter?" Journal of Neuroscience 35, no. 28 (2015): 10168–71. http://dx.doi.org/10.1523/jneurosci.0524-15.2015.

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Korpi, Esa R., Riikka Mäkelä, and Mikko Uusi-Oukari. "Ethanol: Novel Actions on Nerve Cell Physiology Explain Impaired Functions." Physiology 13, no. 4 (1998): 164–70. http://dx.doi.org/10.1152/physiologyonline.1998.13.4.164.

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Molecular biological tools have revealed receptor proteins for excitatory and inhibitory neurotransmitters on cell membranes as targets of ethanol action. Behavioral and pharmacogenetic assays using rodent lines have supported this neurotransmitter theory of ethanol action and given a firm basis for future identification of the relevant genes and the central physiological processes vulnerable to ethanol.

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Li, Yi-Fan, Keshia L. Jackson, Javier E. Stern, Brandon Rabeler, and Kaushik P. Patel. "Interaction between glutamate and GABA systems in the integration of sympathetic outflow by the paraventricular nucleus of the hypothalamus." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 6 (2006): H2847—H2856. http://dx.doi.org/10.1152/ajpheart.00625.2005.

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The paraventricular nucleus (PVN) of the hypothalamus is a central site known to modulate sympathetic outflow. Excitatory and inhibitory neurotransmitters within the PVN dictate final outflow. The goal of the present study was to examine the role of the interaction between the excitatory neurotransmitter glutamate and the inhibitory neurotransmitter GABA in the regulation of sympathetic activity. In α-chloralose- and urethane-anesthetized rats, microinjection of glutamate and N-methyl-d-aspartate (NMDA; 50, 100, and 200 pmol) into the PVN produced dose-dependent increases in renal sympathetic

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Patel, Piyush M., John C. Drummond, Daniel J. Cole, and Randall L. Goskowicz. "Isoflurane Reduces Ischemia-induced Glutamate Release in Rats Subjected to Forebrain Ischemia." Anesthesiology 82, no. 4 (1995): 996–1003. http://dx.doi.org/10.1097/00000542-199504000-00024.

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Background The release of excitatory neurotransmitters during ischemia is thought to contribute to ischemic neuronal injury. Volatile anesthetics have been shown to reduce excitatory neurotransmission in vitro, and it is conceivable that they reduce ischemia-induced neurotransmitter release. The current investigation was conducted to evaluate the effect of isoflurane and N2O-fentanyl anesthesia on ischemia-induced glutamate release in the rat and to compare it with that of mild hypothermia, an intervention known to reduce glutamate release significantly. Methods Microdialysis probes were impla

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Bickler, Philip E., Leslie T. Buck, and John R. Feiner. "Volatile and Intravenous Anesthetics Decrease Glutamate Release from Cortical Brain Slices during Anoxia." Anesthesiology 83, no. 6 (1995): 1233–40. http://dx.doi.org/10.1097/00000542-199512000-00014.

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Abstract Background Extracellular accumulation of the excitatory neurotransmitter L-glutamate during cerebral hypoxia or ischemia contributes to neuronal death. Anesthetics inhibit release of synaptic neurotransmitters but it is unknown if they alter net extrasynaptic glutamate release, which accounts for most of the glutamate released during hypoxia or ischemia. The purpose of this study was to determine if different types of anesthetics decrease hypoxia-induced glutamate release from rat brain slices.

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Vanden Berghe, Pieter, Sander Molhoek, Ludwig Missiaen, Jan Tack, and Jozef Janssens. "Differential Ca2+ signaling characteristics of inhibitory and excitatory myenteric motor neurons in culture." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 5 (2000): G1121—G1127. http://dx.doi.org/10.1152/ajpgi.2000.279.5.g1121.

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Physiological studies on functionally identified myenteric neurons are scarce because of technical limitations. We combined retrograde labeling, cell culturing, and fluorescent intracellular Ca2+ concentration ([Ca2+]i) signaling to study excitatory neurotransmitter responsiveness of myenteric motor neurons. 1,1-Didodecyl-3,3,3′,3′-tetramethyl indocarbocyanine (DiI) was used to label circular muscle motor neurons of the guinea pig ileum. DiI-labeled neurons were easily detectable in cultures prepared from these segments. The excitatory neurotransmitters (10−5 M) acetylcholine, substance P, and

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10

Puia, Giulia. "The inhibitory action of an excitatory neurotransmitter." Trends in Pharmacological Sciences 23, no. 2 (2002): 57. http://dx.doi.org/10.1016/s0165-6147(02)01976-4.

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11

Tsai, Guochuan. "Abnormal Excitatory Neurotransmitter Metabolism in Schizophrenic Brains." Archives of General Psychiatry 52, no. 10 (1995): 829. http://dx.doi.org/10.1001/archpsyc.1995.03950220039008.

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12

Xin, Haolin, Ying Cui, Zhongping An, Qian Yang, Xuan Zou, and Ning Yu. "Attenuated glutamate induced ROS production by antioxidative compounds in neural cell lines." RSC Advances 9, no. 60 (2019): 34735–43. http://dx.doi.org/10.1039/c9ra03848e.

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Nilsson, G. E., and P. L. Lutz. "Release of inhibitory neurotransmitters in response to anoxia in turtle brain." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 1 (1991): R32—R37. http://dx.doi.org/10.1152/ajpregu.1991.261.1.r32.

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In mammals a massive release of the excitatory neurotransmitter glutamate, occurring within a few minutes of anoxia/ischemia, is thought to be a major mediator of anoxic brain damage. In contrast to the mammalian brain, the turtle brain is exceptionally anoxia tolerant. Using intracerebral microdialysis in turtle brain striatum, we have found a large increase in the extracellular level of the inhibitory neurotransmitter gamma-aminobutyric acid during anoxia, reaching 90 times the normoxic level after 240 min, whereas no substantial release of glutamate occurred. Moreover, the inhibitory neurot

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Liu, Lin. "Toxicity of Pesticide on Neurotransmitter." Advanced Materials Research 518-523 (May 2012): 2045–48. http://dx.doi.org/10.4028/www.scientific.net/amr.518-523.2045.

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Pesticides not only play an important role in development of agricultural in China, but also bring much neurotoxicity on the safety of human by intervention compound, analyze and metabolize of neurotransmitter. Many pesticides have neurotransmitter toxicity, including inhibition of cholinesterase activity, increasing excitatory amino acid, decreasing the level of Dopamine. The paper made a brief overview on the toxicity of pesticides on neurotransmitter.

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Bertels, Hannah, Guillem Vicente-Ortiz, Khadija El Kanbi, and Aya Takeoka. "Neurotransmitter phenotype switching by spinal excitatory interneurons regulates locomotor recovery after spinal cord injury." Nature Neuroscience 25, no. 5 (2022): 617–29. http://dx.doi.org/10.1038/s41593-022-01067-9.

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AbstractSevere spinal cord injury in adults leads to irreversible paralysis below the lesion. However, adult rodents that received a complete thoracic lesion just after birth demonstrate proficient hindlimb locomotion without input from the brain. How the spinal cord achieves such striking plasticity remains unknown. In this study, we found that adult spinal cord injury prompts neurotransmitter switching of spatially defined excitatory interneurons to an inhibitory phenotype, promoting inhibition at synapses contacting motor neurons. In contrast, neonatal spinal cord injury maintains the excit

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Harper, Andrew, William R. Blythe, Carlton J. Zdanski, Jiri Prazma, and Harold C. Pillsbury. "Student Research Award 1994: Nitric Oxide in the Rat Vestibular System." Otolaryngology–Head and Neck Surgery 111, no. 4 (1994): 430–38. http://dx.doi.org/10.1177/019459989411100407.

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Nitric oxide is known to function as a neurotransmitter in the central nervous system. It is also known to be involved in the control nervous system excitatory amino acid neurotransmission cascade. Activation of excitatory amino acid receptors causes an influx of calcium, which activates nitric oxide synthase. The resulting increase in intracellular nitric oxide activates soluble guanylate cyclase, leading to a rise in cyclic guanosine monophosphate. The excitatory amino acids giutamate and aspartate are found in the vestibular system and have been postulated to function as vestibular system n

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Rodrigues, Serafim, Mathieu Desroches, Martin Krupa, Jesus M. Cortes, Terrence J. Sejnowski, and Afia B. Ali. "Time-coded neurotransmitter release at excitatory and inhibitory synapses." Proceedings of the National Academy of Sciences 113, no. 8 (2016): E1108—E1115. http://dx.doi.org/10.1073/pnas.1525591113.

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Communication between neurons at chemical synapses is regulated by hundreds of different proteins that control the release of neurotransmitter that is packaged in vesicles, transported to an active zone, and released when an input spike occurs. Neurotransmitter can also be released asynchronously, that is, after a delay following the spike, or spontaneously in the absence of a stimulus. The mechanisms underlying asynchronous and spontaneous neurotransmitter release remain elusive. Here, we describe a model of the exocytotic cycle of vesicles at excitatory and inhibitory synapses that accounts

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Weinberg, Richard J. "Glutamate: an excitatory neurotransmitter in the mammalian CNS." Brain Research Bulletin 50, no. 5-6 (1999): 353–54. http://dx.doi.org/10.1016/s0361-9230(99)00102-1.

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Khanin, Raya, Hanna Parnas, and Lee Segel. "A Mechanism for Discharge of Charged Excitatory Neurotransmitter." Biophysical Journal 72, no. 2 (1997): 507–21. http://dx.doi.org/10.1016/s0006-3495(97)78691-0.

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Yang, Yongjie, Oguz Gozen, Andrew Watkins, et al. "Presynaptic Regulation of Astroglial Excitatory Neurotransmitter Transporter GLT1." Neuron 61, no. 6 (2009): 880–94. http://dx.doi.org/10.1016/j.neuron.2009.02.010.

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Reyes, Nicolas, Juan Carlos Canul Tec, Reda Assal, et al. "Novel Molecular Mechanism of Excitatory Neurotransmitter Transport Inhibition." Biophysical Journal 112, no. 3 (2017): 13a. http://dx.doi.org/10.1016/j.bpj.2016.11.101.

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Vandenberg, Robert J., Pengchu Ju, Karin R. Aubrey, Renae M. Ryan, and Ann D. Mitrovic. "Allosteric modulation of neurotransmitter transporters at excitatory synapses." European Journal of Pharmaceutical Sciences 23, no. 1 (2004): 1–11. http://dx.doi.org/10.1016/j.ejps.2004.05.006.

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Li, Fei, Jacob Eriksen, Janet Finer-Moore, et al. "Ion transport and regulation in a synaptic vesicle glutamate transporter." Science 368, no. 6493 (2020): 893–97. http://dx.doi.org/10.1126/science.aba9202.

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Synaptic vesicles accumulate neurotransmitters, enabling the quantal release by exocytosis that underlies synaptic transmission. Specific neurotransmitter transporters are responsible for this activity and therefore are essential for brain function. The vesicular glutamate transporters (VGLUTs) concentrate the principal excitatory neurotransmitter glutamate into synaptic vesicles, driven by membrane potential. However, the mechanism by which they do so remains poorly understood owing to a lack of structural information. We report the cryo–electron microscopy structure of rat VGLUT2 at 3.8-angs

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Trudeau, L. E., and V. F. Castellucci. "Excitatory amino acid neurotransmission at sensory-motor and interneuronal synapses of Aplysia californica." Journal of Neurophysiology 70, no. 3 (1993): 1221–30. http://dx.doi.org/10.1152/jn.1993.70.3.1221.

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1. Although the gill and siphon withdrawal reflex of Aplysia has been used as a model system to study learning-associated changes in synaptic transmission, the identity of the neurotransmitter released by the sensory neurons and excitatory interneurons of the network mediating this behavior is still unknown. The identification of the putative neurotransmitter of these neurons should facilitate further studies of synaptic plasticity in Aplysia. 2. We report that sensory-motor transmission within this circuit is mediated through the activation of an excitatory amino acid receptor that is blocked

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Chandana, Bandaru, G. Krishna Mohan, and M. Sandhya Rani. "Advanced Molecular Mechanisms of Epilepsy." Journal of Pharmaceutical Quality Assurance and Quality Control 5, no. 2 (2023): 22–34. http://dx.doi.org/10.46610/jqaqc.2023.v05i02.004.

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The Central Nervous System (CNS) is a complex network composed of the cerebral cortex and the vertebral column, orchestrating intricate processes through neural networks and chemical regulation. Neurotransmission in the CNS involves neurotransmitters, neuromodulators, neuromediators, and neurotropic factors, playing distinct roles in cellular activity and synaptic plasticity. Various neurotransmitters such as dopamine, glutamate, GABA, glycine, serotonin, and others exert diverse effects on the CNS through specific receptors, influencing synaptic transmission and neuronal excitability. GABA, t

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Mohammadzadeh Jahani, Peyman, Reza Zaimbashi, Mohammad Reza Aflatoonian, Somayeh Tajik, and Hadi Beitollahi. "Electrochemical sensor for acetylcholine detection based on WO3 nanorods-modified glassy carbon electrode." Journal of Electrochemical Science and Engineering 14, no. 5 (2024): 631–41. http://dx.doi.org/10.5599/jese.2462.

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Acetylcholine (ACH) is one of the excitatory neurotransmitter in the human body. It is the most abundant neurotransmitter responsible for triggering the activation of postsynaptic neurons, leading to an excitatory response. ACH plays a crucial role in various physiological processes, including muscle contraction, autonomic nervous system regulation, and cognitive functions such as learning and memory. In this study, an electrochemical sensor was prepared based on WO3 nanorods modified glassy carbon electrode for the detection of ACH. The WO3 nanorods provided excellent properties for the elect

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Sedlak, Thomas W., Bindu D. Paul, Gregory M. Parker, et al. "The glutathione cycle shapes synaptic glutamate activity." Proceedings of the National Academy of Sciences 116, no. 7 (2019): 2701–6. http://dx.doi.org/10.1073/pnas.1817885116.

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Glutamate is the most abundant excitatory neurotransmitter, present at the bulk of cortical synapses, and participating in many physiologic and pathologic processes ranging from learning and memory to stroke. The tripeptide, glutathione, is one-third glutamate and present at up to low millimolar intracellular concentrations in brain, mediating antioxidant defenses and drug detoxification. Because of the substantial amounts of brain glutathione and its rapid turnover under homeostatic control, we hypothesized that glutathione is a relevant reservoir of glutamate and could influence synaptic exc

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Sánchez Fernández, Iván, and Tobias Loddenkemper. "Subunit Composition of Neurotransmitter Receptors in the Immature and in the Epileptic Brain." BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/301950.

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Neuronal activity is critical for synaptogenesis and the development of neuronal networks. In the immature brain excitation predominates over inhibition facilitating the development of normal brain circuits, but also rendering it more susceptible to seizures. In this paper, we review the evolution of the subunit composition of neurotransmitter receptors during development, how it promotes excitation in the immature brain, and how this subunit composition of neurotransmission receptors may be also present in the epileptic brain. During normal brain development, excitatory glutamate receptors pe

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Snyder, G. L., G. Fisone, P. Morino, et al. "Regulation by the neuropeptide cholecystokinin (CCK-8S) of protein phosphorylation in the neostriatum." Proceedings of the National Academy of Sciences 90, no. 23 (1993): 11277–81. http://dx.doi.org/10.1073/pnas.90.23.11277.

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Despite physiological evidence that cholecystokinin (CCK) is an excitatory neurotransmitter in the brain, little is known about its mechanism of action. CCK immunoreactivity in the brain, including projections to the striatum, is primarily attributable to the sulfated octapeptide CCK-8S. We report here that CCK-8S abolishes cAMP-dependent phosphorylation of a dopamine- and cAMP-regulated 32-kDa phosphoprotein (DARPP-32) in striatal neurons. The effect of CCK-8S is prevented by antagonists of CCKB and N-methyl-D-aspartate receptors. Our results support a model in which CCK-8S, originating from

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Saleh, T. M., and D. F. Cechetto. "Neurochemical interactions in the parabrachial nucleus mediating visceral inputs to visceral thalamic neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 3 (1995): R786—R795. http://dx.doi.org/10.1152/ajpregu.1995.268.3.r786.

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Previously we demonstrated that glutamatergic and noradrenergic receptors mediate the relay of visceral information through the parabrachial nucleus (PBN) and that calcitonin gene-related peptide (CGRP), substance P (SP), somatostatin (SOM), neurotensin (NT), and cholecystokinin (CCK) may modulate these responses. The interactions of these neurotransmitters and neuropeptides were examined in male Wistar rats (17) that were anesthetized with chloral hydrate and ventilated and in which blood pressure and heart rate were continuously monitored. The left cervical vagus nerve was stimulated at subm

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Song, Jiayi, Xuehan Yang, Ming Zhang, Chunyan Wang, and Li Chen. "Glutamate Metabolism in Mitochondria is Closely Related to Alzheimer’s Disease." Journal of Alzheimer's Disease 84, no. 2 (2021): 557–78. http://dx.doi.org/10.3233/jad-210595.

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Glutamate is the main excitatory neurotransmitter in the brain, and its excitatory neurotoxicity is closely related to the occurrence and development of Alzheimer’s disease. However, increasing evidence shows that in the process of Alzheimer’s disease, glutamate is not only limited to its excitotoxicity as a neurotransmitter but also related to the disorder of its metabolic balance. The balance of glutamate metabolism in the brain is an important determinant of central nervous system health, and the maintenance of this balance is closely related to glutamate uptake, glutamate circulation, intr

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Sharp, Sally I., Paul T. Francis, and Clive G. Ballard. "Neurochemistry of severe dementia." Reviews in Clinical Gerontology 15, no. 2 (2005): 105–23. http://dx.doi.org/10.1017/s0959259805001681.

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Severe dementia is associated with frequent psychiatric and behavioural disturbances in addition to marked cognitive and functional deficits. Research to determine a neurochemical understanding of dementia over the last three decades has generated therapeutic strategies which improve patients' cognition and activities of daily living. Different key dementia syndromes have been shown to have distinct neurotransmitter biochemical patho-logy, with important implications for therapy. The current review focuses predominantly upon excitatory neurotransmitter systems.

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Varinthra, Peeraporn, Shameemun Naseer Mohamed Nizarul Anwar, Shu-Ching Shih, and Ingrid Y. Liu. "The role of the GABAergic system on insomnia." Tzu Chi Medical Journal 36, no. 2 (2024): 103–9. http://dx.doi.org/10.4103/tcmj.tcmj_243_23.

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Sleep is an essential activity for the survival of mammals. Good sleep quality helps promote the performance of daily functions. In contrast, insufficient sleep reduces the efficiency of daily activities, causes various chronic diseases like Alzheimer’s disease, and increases the risk of having accidents. The GABAergic system is the primary inhibitory neurotransmitter system in the central nervous system. It transits the gamma-aminobutyric acid (GABA) neurotransmitter via GABAA and GABAB receptors to counterbalance excitatory neurotransmitters, such as glutamate, noradrenaline, serotonin, acet

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Li, Z., and A. V. Ferguson. "Subfornical organ efferents to paraventricular nucleus utilize angiotensin as a neurotransmitter." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 2 (1993): R302—R309. http://dx.doi.org/10.1152/ajpregu.1993.265.2.r302.

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In this study, we have utilized electrophysiological single unit recordings to evaluate the effects of nonpeptidergic angiotensin II (ANG II) antagonists on neural responses of hypothalamic paraventricular nucleus (PVN) neurons to either electrical stimulation in subfornical organ (SFO) or direct application of ANG II. Electrical stimulation (200-400 microA; 0.1 ms) in the SFO resulted in excitatory responses in 36 of 50 PVN neurons tested. Peristimulus histogram analysis of such excitatory effects demonstrated latencies of < 30 ms and variability of response times of approximately 50 ms in

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Tang, CM, QY Shi, A. Katchman, and G. Lynch. "Modulation of the time course of fast EPSCs and glutamate channel kinetics by aniracetam." Science 254, no. 5029 (1991): 288–90. http://dx.doi.org/10.1126/science.254.5029.288.

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It is generally accepted that glutamate serves as the neurotransmitter at most excitatory synapses in the mammalian central nervous system (CNS). Synaptic release of glutamate may trigger a fast and a slow excitatory postsynaptic current (EPSC). The slow EPSC is mediated by N-methyl-D-aspartate (NMDA) receptor channels, whereas the fast EPSC is mediated by non-NMDA receptor channels. The nootropic agent aniracetam selectively and reversibly slows the desensitization kinetics of non-NMDA channels and lengthens their single-channel open times. Antiracetam also modulates the kinetics of the fast

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Watkins, J. C. "l-Glutamate as a Central Neurotransmitter: Looking Back." Biochemical Society Transactions 28, no. 4 (2000): 297–310. http://dx.doi.org/10.1042/bst0280297.

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The high concentration in brain of unbound l-glutamic acid (in its anionic form, l-glutamate) fuelled considerable speculation as to its role in central nervous function more than 50 years ago. Claims in the 1940s that it could improve cognitive acuity in patients with mental impairment were particularly intriguing, though later refuted. In the early 1950s Hayashi [(1954) Keio J. Med. 3, 183–192] found that l-glutamate could cause convulsions and proposed that it might be a central synaptic transmitter. Soon thereafter, Curtis and colleagues [Curtis, Phillis and Watkins (1959) Nature (London)

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Takeuchi, Tatsuto, Sanae Yoshimoto, Yasuhiro Shimada, Takanori Kochiyama, and Hirohito M. Kondo. "Individual differences in visual motion perception and neurotransmitter concentrations in the human brain." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1714 (2017): 20160111. http://dx.doi.org/10.1098/rstb.2016.0111.

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Recent studies have shown that interindividual variability can be a rich source of information regarding the mechanism of human visual perception. In this study, we examined the mechanisms underlying interindividual variability in the perception of visual motion, one of the fundamental components of visual scene analysis, by measuring neurotransmitter concentrations using magnetic resonance spectroscopy. First, by psychophysically examining two types of motion phenomena—motion assimilation and contrast—we found that, following the presentation of the same stimulus, some participants perceived

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Olsen, Olav, Kimberly A. Moore, Masaki Fukata та ін. "Neurotransmitter release regulated by a MALS–liprin-α presynaptic complex". Journal of Cell Biology 170, № 7 (2005): 1127–34. http://dx.doi.org/10.1083/jcb.200503011.

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Synapses are highly specialized intercellular junctions organized by adhesive and scaffolding molecules that align presynaptic vesicular release with postsynaptic neurotransmitter receptors. The MALS/Veli–CASK–Mint-1 complex of PDZ proteins occurs on both sides of the synapse and has the potential to link transsynaptic adhesion molecules to the cytoskeleton. In this study, we purified the MALS protein complex from brain and found liprin-α as a major component. Liprin proteins organize the presynaptic active zone and regulate neurotransmitter release. Fittingly, mutant mice lacking all three MA

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Foxx-Orenstein, A. E., and J. R. Grider. "Regulation of colonic propulsion by enteric excitatory and inhibitory neurotransmitters." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 3 (1996): G433—G437. http://dx.doi.org/10.1152/ajpgi.1996.271.3.g433.

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The contribution of excitatory and inhibitory motor neurotransmitters to colonic propulsion was examined in isolated segments of guinea pig colon. Synthetic fecal pellets were inserted at the proximal end of the segment, and the velocity of pellet propulsion across a fixed distance was measured in the presence and absence of selective neurotransmitter antagonists. The control velocity (0.97 +/- 0.02 mm/s) was inhibited in a concentration-dependent fashion by atropine and the neurokinin (NK)-2a antagonist MEN-10,376 [half-maximal inhibitory concentration (IC50), 1 microM; maximal inhibition, 98

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Nurse, Colin A., Erin M. Leonard, and Shaima Salman. "Role of glial-like type II cells as paracrine modulators of carotid body chemoreception." Physiological Genomics 50, no. 4 (2018): 255–62. http://dx.doi.org/10.1152/physiolgenomics.00142.2017.

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Mammalian carotid bodies (CB) are chemosensory organs that mediate compensatory cardiorespiratory reflexes in response to low blood PO2 (hypoxemia) and elevated CO2/H+ (acid hypercapnia). The chemoreceptors are glomus or type I cells that occur in clusters enveloped by neighboring glial-like type II cells. During chemoexcitation type I cells depolarize, leading to Ca2+-dependent release of several neurotransmitters, some excitatory and others inhibitory, that help shape the afferent carotid sinus nerve (CSN) discharge. Among the predominantly excitatory neurotransmitters are the purines ATP an

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Divakaruni, Ajit S., Martina Wallace, Caodu Buren, et al. "Inhibition of the mitochondrial pyruvate carrier protects from excitotoxic neuronal death." Journal of Cell Biology 216, no. 4 (2017): 1091–105. http://dx.doi.org/10.1083/jcb.201612067.

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Glutamate is the dominant excitatory neurotransmitter in the brain, but under conditions of metabolic stress it can accumulate to excitotoxic levels. Although pharmacologic modulation of excitatory amino acid receptors is well studied, minimal consideration has been given to targeting mitochondrial glutamate metabolism to control neurotransmitter levels. Here we demonstrate that chemical inhibition of the mitochondrial pyruvate carrier (MPC) protects primary cortical neurons from excitotoxic death. Reductions in mitochondrial pyruvate uptake do not compromise cellular energy metabolism, sugges

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Monday, Hannah R., Thomas J. Younts, and Pablo E. Castillo. "Long-Term Plasticity of Neurotransmitter Release: Emerging Mechanisms and Contributions to Brain Function and Disease." Annual Review of Neuroscience 41, no. 1 (2018): 299–322. http://dx.doi.org/10.1146/annurev-neuro-080317-062155.

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Long-lasting changes of brain function in response to experience rely on diverse forms of activity-dependent synaptic plasticity. Chief among them are long-term potentiation and long-term depression of neurotransmitter release, which are widely expressed by excitatory and inhibitory synapses throughout the central nervous system and can dynamically regulate information flow in neural circuits. This review article explores recent advances in presynaptic long-term plasticity mechanisms and contributions to circuit function. Growing evidence indicates that presynaptic plasticity may involve struc

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Khakhalin, Arseny S. "Questioning the depolarizing effects of GABA during early brain development." Journal of Neurophysiology 106, no. 3 (2011): 1065–67. http://dx.doi.org/10.1152/jn.00293.2011.

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During early brain development, γ-aminobutyric acid (GABA), the main inhibitory neurotransmitter in the adult brain, has been thought to be an important source of excitatory neurotransmission. This view, however, was recently challenged by a series of studies that claim that the excitatory effect of GABA is due to non-physiological in vitro experimental conditions. In this article, we aim to summarize results that support and challenge the traditional point of view, and indicate some strong and weak points of both positions.

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Zhou, Wei, Liang-Wu Fu, Stephanie C. Tjen-A-Looi, Zhi-ling Guo, and John C. Longhurst. "Role of glutamate in a visceral sympathoexcitatory reflex in rostral ventrolateral medulla of cats." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 3 (2006): H1309—H1318. http://dx.doi.org/10.1152/ajpheart.00202.2006.

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The rostral ventrolateral medulla (rVLM) is involved in processing visceral sympathetic reflexes. However, there is little information on specific neurotransmitters in this brain stem region involved in this reflex. The present study investigated the importance of glutamate and glutamatergic receptors in the rVLM during gallbladder stimulation with bradykinin (BK), because glutamate is thought to function as an excitatory neurotransmitter in this region. Stimulation of visceral afferents activated glutamatergic neurons in the rVLM, as noted by double-labeling with c-Fos and the cellular vesicu

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Hira, Zameer, Iqbal Mehrunisa, Anwer Lubna, Ahmed Sadaf, and Mushtaq Samia. "Comparative effects of caffeine & L-Theanine consumption on subjective cardiovascular signs and Neurophysiological responses." International Journal of Endorsing Health Science Research 1, no. 1 (2013): 38–42. https://doi.org/10.29052/IJEHSR.v1.i1.2013.38-42.

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Abstract Non-alcoholic beverages comprise of Caffeine and L-theanine as core ingredients. Caffeine is attributed to augment cardiovascular and neurophysiological responses by enhancing the neurotransmission of catecholamines after binding with adenosine receptors antagonistically. L-theanine, as a constituent of green tea is helpful in lowering blood pressure by antagonizing the effects of excitatory neurotransmitters after subsequent release of inhibitory neurotransmitter GABA. 87 healthy females with age 18-19 years, participated in the study were divided into three different groups. Group A

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He, Yu-Hui, Ling Li, Xu-Fang Liang, Shan He, Luo Zhao, and Yan-Peng Zhang. "Inhibitory neurotransmitter serotonin and excitatory neurotransmitter dopamine both decrease food intake in Chinese perch (Siniperca chuatsi)." Fish Physiology and Biochemistry 44, no. 1 (2017): 175–83. http://dx.doi.org/10.1007/s10695-017-0422-8.

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Liguz-Lecznar, Monika, and Jolanta Skangiel-Kramska. "Vesicular glutamate transporters (VGLUTs): The three musketeers of glutamatergic system." Acta Neurobiologiae Experimentalis 67, no. 3 (2007): 207–18. http://dx.doi.org/10.55782/ane-2007-1649.

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Glutamate is the predominant excitatory neurotransmitter in the central nervous system (CNS) and glutamatergic transmission is critical for controlling neuronal activity. Glutamate is stored in synaptic vesicles and released upon stimulation. The homeostasis of glutamatergic system is maintained by a set of transporters present in plasma membrane and in the membrane of synaptic vesicles. The family of vesicular glutamate transporters in mammals is comprised of three highly homologous proteins: VGLUT1-3. The expression of particular VGLUTs is largely complementary with limited overlap and so fa

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Lutz, P. L., and R. Reiners. "Survival of energy failure in the anoxic frog brain: delayed release of glutamate." Journal of Experimental Biology 200, no. 22 (1997): 2913–17. http://dx.doi.org/10.1242/jeb.200.22.2913.

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This study investigated the relationship between energy failure and neurotransmitter release in the frog (Rana pipiens) brain during 1-3 h of anoxia. Unlike truly anoxia-tolerant species, the frog does not defend its brain energy charge. When exposed to anoxia at 25 degrees C, there is an immediate fall in brain ATP levels, which reach approximately 20% of normoxic levels in approximately 60 min. The frog, nevertheless, survives another 1-2 h of anoxia. At 100 min of anoxia, there is an increase in extracellular adenosine concentration, probably originating from the increased intracellular ade

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Wang, Wenping, Ximing Wu, Chung S. Yang, and Jinsong Zhang. "An Unrecognized Fundamental Relationship between Neurotransmitters: Glutamate Protects against Catecholamine Oxidation." Antioxidants 10, no. 10 (2021): 1564. http://dx.doi.org/10.3390/antiox10101564.

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Neurotransmitter catecholamines (dopamine, epinephrine, and norepinephrine) are liable to undergo oxidation, which copper is deeply involved in. Catecholamine oxidation-derived neurotoxicity is recognized as a pivotal pathological mechanism in neurodegenerative diseases. Glutamate, as an excitatory neurotransmitter, is enriched in the brain at extremely high concentrations. However, the chemical biology relationship of these two classes of neurotransmitters remains largely unknown. In the present study, we assessed the influences of glutamate on the autoxidation of catecholamines, the copper-

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Neuray, Caroline, Reza Maroofian, Marcello Scala, et al. "Early-infantile onset epilepsy and developmental delay caused by bi-allelic GAD1 variants." Brain 143, no. 8 (2020): 2388–97. http://dx.doi.org/10.1093/brain/awaa178.

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Abstract Gamma-aminobutyric acid (GABA) and glutamate are the most abundant amino acid neurotransmitters in the brain. GABA, an inhibitory neurotransmitter, is synthesized by glutamic acid decarboxylase (GAD). Its predominant isoform GAD67, contributes up to ∼90% of base-level GABA in the CNS, and is encoded by the GAD1 gene. Disruption of GAD1 results in an imbalance of inhibitory and excitatory neurotransmitters, and as Gad1−/− mice die neonatally of severe cleft palate, it has not been possible to determine any potential neurological dysfunction. Furthermore, little is known about the conse

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