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Journal articles on the topic 'Parvalbumin positive interneuron'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Cooke, James E., Martin C. Kahn, Edward O. Mann, Andrew J. King, Jan W. H. Schnupp, and Ben D. B. Willmore. "Contrast gain control occurs independently of both parvalbumin-positive interneuron activity and shunting inhibition in auditory cortex." Journal of Neurophysiology 123, no. 4 (2020): 1536–51. http://dx.doi.org/10.1152/jn.00587.2019.

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We investigated whether contrast gain control is mediated by shunting inhibition from parvalbumin-positive interneurons in auditory cortex. We performed extracellular and intracellular recordings in mouse auditory cortex while presenting sensory stimuli with varying contrasts and manipulated parvalbumin-positive interneuron activity using optogenetics. We show that while parvalbumin-positive interneuron activity modulates the gain of cortical responses, this activity is not the primary mechanism for contrast gain control in auditory cortex.

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2

Woodruff, Alan R., and Pankaj Sah. "Inhibition and Synchronization of Basal Amygdala Principal Neuron Spiking by Parvalbumin-Positive Interneurons." Journal of Neurophysiology 98, no. 5 (2007): 2956–61. http://dx.doi.org/10.1152/jn.00739.2007.

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Using mice that express enhance green fluorescent protein (EGFP) under the control of the parvalbumin promoter, we made paired recordings from interneurons and principal neurons in the basal amygdala. In synaptically connected pairs, we show that single action potentials in a parvalbumin expressing interneuron can inhibit spiking in the synaptically connected principal neuron. When principal neurons were provided with suprathreshold oscillatory drive via a somatic patch pipette, action potentials in the interneuron inhibited spiking in principal neurons only when the interneuron spike occurred

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3

Giesers, Naomi K., and Oliver Wirths. "Loss of Hippocampal Calretinin and Parvalbumin Interneurons in the 5XFAD Mouse Model of Alzheimer’s Disease." ASN Neuro 12 (January 2020): 175909142092535. http://dx.doi.org/10.1177/1759091420925356.

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The deposition of amyloid-β peptides in the form of extracellular plaques and neuronal degeneration belong to the hallmark features of Alzheimer’s disease (AD). In addition, impaired calcium homeostasis and altered levels in calcium-binding proteins seem to be associated with the disease process. In this study, calretinin- (CR) and parvalbumin- (PV) positive gamma-aminobutyric acid-producing (GABAergic) interneurons were quantified in different hippocampal subfields of 12-month-old wild-type mice, as well as in the transgenic AD mouse models 5XFAD and Tg4-42. While, in comparison with wild-typ

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Howard, MacKenzie A., and Scott C. Baraban. "Synaptic integration of transplanted interneuron progenitor cells into native cortical networks." Journal of Neurophysiology 116, no. 2 (2016): 472–78. http://dx.doi.org/10.1152/jn.00321.2016.

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Interneuron-based cell transplantation is a powerful method to modify network function in a variety of neurological disorders, including epilepsy. Whether new interneurons integrate into native neural networks in a subtype-specific manner is not well understood, and the therapeutic mechanisms underlying interneuron-based cell therapy, including the role of synaptic inhibition, are debated. In this study, we tested subtype-specific integration of transplanted interneurons using acute cortical brain slices and visualized patch-clamp recordings to measure excitatory synaptic inputs, intrinsic pro

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Hameed, Mustafa Q., Tsung-Hsun Hsieh, Leon Morales-Quezada, et al. "Ceftriaxone Treatment Preserves Cortical Inhibitory Interneuron Function via Transient Salvage of GLT-1 in a Rat Traumatic Brain Injury Model." Cerebral Cortex 29, no. 11 (2018): 4506–18. http://dx.doi.org/10.1093/cercor/bhy328.

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Abstract Traumatic brain injury (TBI) results in a decrease in glutamate transporter-1 (GLT-1) expression, the major mechanism for glutamate removal from synapses. Coupled with an increase in glutamate release from dead and dying neurons, this causes an increase in extracellular glutamate. The ensuing glutamate excitotoxicity disproportionately damages vulnerable GABAergic parvalbumin-positive inhibitory interneurons, resulting in a progressively worsening cortical excitatory:inhibitory imbalance due to a loss of GABAergic inhibitory tone, as evidenced by chronic post-traumatic symptoms such a

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Sherwood, Chet C., Mary Ann Raghanti, Cheryl D. Stimpson, et al. "Inhibitory interneurons of the human prefrontal cortex display conserved evolution of the phenotype and related genes." Proceedings of the Royal Society B: Biological Sciences 277, no. 1684 (2009): 1011–20. http://dx.doi.org/10.1098/rspb.2009.1831.

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Inhibitory interneurons participate in local processing circuits, playing a central role in executive cognitive functions of the prefrontal cortex. Although humans differ from other primates in a number of cognitive domains, it is not currently known whether the interneuron system has changed in the course of primate evolution leading to our species. In this study, we examined the distribution of different interneuron subtypes in the prefrontal cortex of anthropoid primates as revealed by immunohistochemistry against the calcium-binding proteins calbindin, calretinin and parvalbumin. In additi

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Yekhlef, Latefa, Gian Luca Breschi, Laura Lagostena, Giovanni Russo, and Stefano Taverna. "Selective activation of parvalbumin- or somatostatin-expressing interneurons triggers epileptic seizurelike activity in mouse medial entorhinal cortex." Journal of Neurophysiology 113, no. 5 (2015): 1616–30. http://dx.doi.org/10.1152/jn.00841.2014.

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GABAergic interneurons are thought to play a critical role in eliciting interictal spikes (IICs) and triggering ictal discharges in temporal lobe epilepsy, yet the contribution of different interneuronal subtypes to seizure initiation is still largely unknown. Here we took advantage of optogenetic techniques combined with patch-clamp and field recordings to selectively stimulate parvalbumin (PV)- or somatostatin (SOM)-positive interneurons expressing channelrhodopsin-2 (CHR-2) in layers II–III of adult mouse medial entorhinal cortical slices during extracellular perfusion with the proconvulsiv

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8

Negwer, Moritz, Karol Piera, Rick Hesen, et al. "EHMT1 regulates Parvalbumin-positive interneuron development and GABAergic input in sensory cortical areas." Brain Structure and Function 225, no. 9 (2020): 2701–16. http://dx.doi.org/10.1007/s00429-020-02149-9.

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AbstractMutations in the Euchromatic Histone Methyltransferase 1 (EHMT1) gene cause Kleefstra syndrome, a rare form of intellectual disability (ID) with strong autistic traits and sensory processing deficits. Proper development of inhibitory interneurons is crucial for sensory function. Here we report a timeline of Parvalbumin-positive (PV+) interneuron development in the three most important sensory cortical areas in the Ehmt1+/− mouse. We find a hitherto unreported delay of PV+ neuron maturation early in sensory development, with layer- and region-specific variability later in development. T

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Singh, Yajuvinder, Henri Leinonen, Feroze Fazaludeen, et al. "Loss of Cln5 leads to altered Gad1 expression and deficits in interneuron development in mice." Human Molecular Genetics 28, no. 19 (2019): 3309–22. http://dx.doi.org/10.1093/hmg/ddz165.

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Abstract The Finnish-variant late infantile neuronal ceroid lipofuscinosis, also known as CLN5 disease, is caused by mutations in the CLN5 gene. Cln5 is strongly expressed in the developing brain and expression continues into adulthood. CLN5, a protein of unknown function, is implicated in neurodevelopment but detailed investigation is lacking. Using Cln5−/− embryos of various ages and cells harvested from Cln5−/− brains we investigated the hitherto unknown role of Cln5 in the developing brain. Loss of Cln5 results in neuronal differentiation deficits and delays in interneuron development duri

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Selten, Martijn, Hans van Bokhoven, and Nael Nadif Kasri. "Inhibitory control of the excitatory/inhibitory balance in psychiatric disorders." F1000Research 7 (January 8, 2018): 23. http://dx.doi.org/10.12688/f1000research.12155.1.

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Neuronal networks consist of different types of neurons that all play their own role in order to maintain proper network function. The two main types of neurons segregate in excitatory and inhibitory neurons, which together regulate the flow of information through the network. It has been proposed that changes in the relative strength in these two opposing forces underlie the symptoms observed in psychiatric disorders, including autism and schizophrenia. Here, we review the role of alterations to the function of the inhibitory system as a cause of psychiatric disorders. First, we explore both

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Cisneros-Franco, J. Miguel, and Étienne de Villers-Sidani. "Reactivation of critical period plasticity in adult auditory cortex through chemogenetic silencing of parvalbumin-positive interneurons." Proceedings of the National Academy of Sciences 116, no. 52 (2019): 26329–31. http://dx.doi.org/10.1073/pnas.1913227117.

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Sensory experience during early developmental critical periods (CPs) has profound and long-lasting effects on cortical sensory processing perduring well into adulthood. Although recent evidence has shown that reducing cortical inhibition during adulthood reinstates CP plasticity, the precise cellular mechanisms are not well understood. Here, we show that chemogenetic inactivation of parvalbumin-positive (PV+) interneurons is sufficient to reinstate CP plasticity in the adult auditory cortex. Bidirectional manipulation of PV+cell activity affected neuronal spectral and sound intensity selectivi

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Jang, Hyun Jae, Hyowon Chung, James M. Rowland, Blake A. Richards, Michael M. Kohl, and Jeehyun Kwag. "Distinct roles of parvalbumin and somatostatin interneurons in gating the synchronization of spike times in the neocortex." Science Advances 6, no. 17 (2020): eaay5333. http://dx.doi.org/10.1126/sciadv.aay5333.

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Synchronization of precise spike times across multiple neurons carries information about sensory stimuli. Inhibitory interneurons are suggested to promote this synchronization, but it is unclear whether distinct interneuron subtypes provide different contributions. To test this, we examined single-unit recordings from barrel cortex in vivo and used optogenetics to determine the contribution of parvalbumin (PV)– and somatostatin (SST)–positive interneurons to the synchronization of spike times across cortical layers. We found that PV interneurons preferentially promote the synchronization of sp

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Helm, Jessica, Gulcan Akgul, and Lonnie P. Wollmuth. "Subgroups of parvalbumin-expressing interneurons in layers 2/3 of the visual cortex." Journal of Neurophysiology 109, no. 6 (2013): 1600–1613. http://dx.doi.org/10.1152/jn.00782.2012.

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The input, processing, and output characteristics of inhibitory interneurons help shape information flow through layers 2/3 of the visual cortex. Parvalbumin (PV)-positive interneurons modulate and synchronize the gain and dynamic responsiveness of pyramidal neurons. To define the diversity of PV interneurons in layers 2/3 of the developing visual cortex, we characterized their passive and active membrane properties. Using Ward's and k-means multidimensional clustering, we identified four PV interneuron subgroups. The most notable difference between the subgroups was their firing patterns in r

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Kann, Oliver, Ismini E. Papageorgiou, and Andreas Draguhn. "Highly Energized Inhibitory Interneurons are a Central Element for Information Processing in Cortical Networks." Journal of Cerebral Blood Flow & Metabolism 34, no. 8 (2014): 1270–82. http://dx.doi.org/10.1038/jcbfm.2014.104.

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Gamma oscillations (~30 to 100 Hz) provide a fundamental mechanism of information processing during sensory perception, motor behavior, and memory formation by coordination of neuronal activity in networks of the hippocampus and neocortex. We review the cellular mechanisms of gamma oscillations about the underlying neuroenergetics, i.e., high oxygen consumption rate and exquisite sensitivity to metabolic stress during hypoxia or poisoning of mitochondrial oxidative phosphorylation. Gamma oscillations emerge from the precise synaptic interactions of excitatory pyramidal cells and inhibitory GAB

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Molgaard, Simon, Maj Ulrichsen, Simon Boggild, et al. "Immunohistochemical visualization of mouse interneuron subtypes." F1000Research 3 (October 13, 2014): 242. http://dx.doi.org/10.12688/f1000research.5349.1.

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The activity of excitatory neurons is controlled by a small, but highly diverse population of inhibitory interneurons. These cells show a high level of physiological, morphological and neurochemical heterogeneity, and play highly specific roles in neuronal circuits. In the mammalian hippocampus, these are divided into 21 different subtypes of GABAergic interneurons based on their expression of different markers, morphology and their electrophysiological properties. Ideally, all can be marked using an antibody directed against the inhibitory neurotransmitter GABA, but parvalbumin, calbindin, so

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Molgaard, Simon, Maj Ulrichsen, Simon Boggild, et al. "Immunofluorescent visualization of mouse interneuron subtypes." F1000Research 3 (November 20, 2014): 242. http://dx.doi.org/10.12688/f1000research.5349.2.

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The activity of excitatory neurons is controlled by a highly diverse population of inhibitory interneurons. These cells show a high level of physiological, morphological and neurochemical heterogeneity, and play highly specific roles in neuronal circuits. In the mammalian hippocampus, these are divided into 21 different subtypes of GABAergic interneurons based on their expression of different markers, morphology and their electrophysiological properties. Ideally, all can be marked using an antibody directed against the inhibitory neurotransmitter GABA, but parvalbumin, calbindin, somatostatin,

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Molgaard, Simon, Maj Ulrichsen, Simon Boggild, et al. "Immunofluorescent visualization of mouse interneuron subtypes." F1000Research 3 (June 4, 2015): 242. http://dx.doi.org/10.12688/f1000research.5349.3.

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The activity of excitatory neurons is controlled by a highly diverse population of inhibitory interneurons. These cells show a high level of physiological, morphological and neurochemical heterogeneity, and play highly specific roles in neuronal circuits. In the mammalian hippocampus, these are divided into 21 different subtypes of GABAergic interneurons based on their expression of different markers, morphology and their electrophysiological properties. Ideally, all can be marked using an antibody directed against the inhibitory neurotransmitter GABA, but parvalbumin, calbindin, somatostatin,

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Buia, Calin I., and Paul H. Tiesinga. "Role of Interneuron Diversity in the Cortical Microcircuit for Attention." Journal of Neurophysiology 99, no. 5 (2008): 2158–82. http://dx.doi.org/10.1152/jn.01004.2007.

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Receptive fields of neurons in cortical area V4 are large enough to fit multiple stimuli, making V4 the ideal place to study the effects of selective attention at the single-neuron level. Experiments have revealed evidence for stimulus competition and have characterized the effect thereon of spatial and feature-based attention. We developed a biophysical model with spiking neurons and conductance-based synapses. To account for the comprehensive set of experimental results, it was necessary to include in the model, in addition to regular spiking excitatory (E) cells, two types of interneurons:

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Peng, Hualing, Jie Jia, Yisheng Lu, and Hua Zheng. "Isoflurane Rescue Schizophrenia-Related Deficits through Parvalbumin-Positive Neurons in the Dentate Gyrus." Biomedicines 10, no. 11 (2022): 2759. http://dx.doi.org/10.3390/biomedicines10112759.

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The therapeutic effects of volatile anesthetics on mental diseases, particularly schizophrenia, have gained considerable interest. Although isoflurane is a commonly used volatile anesthetic, there’s no more evidence that it could work on treating schizophrenia. Here, we discovered that inhaling isoflurane at low concentrations might reverse the behavioral phenotypes of schizophrenia caused by MK801, such as hyperlocomotion, pre-pulse inhibition impairment, and working memory loss. Isoflurane also helped recovering adult neurogenesis and synaptic plasticity impairments in the dentate gyrus (DG)

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Dudek, F. Edward. "Selective Inhibitory Interneuron Loss Produces Chronic Hippocampal Hyperexcitability." Epilepsy Currents 2, no. 1 (2002): 21–22. http://dx.doi.org/10.1111/j.1535-7597.2002.00007.x.

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Focal Inhibitory Interneuron Loss and Principal Cell Hyperexcitability in the Rat Hippocampus After Microinjection of a Neurotoxic Conjugate of Saporin and a Peptidase-Resistant Analog of Substance P Martin JL, Sloviter RS J Comp Neurol 2001;436:127–152 Episodes of prolonged seizures or head trauma produce chronic hippocampal network hyperexcitability hypothesized to result primarily from inhibitory interneuron loss or dysfunction. The possibly causal role of inhibitory neuron failure in the development of epileptiform pathophysiology remains unclear because global neurologic injuries produce

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Funk, Marzieh, Stefan Jaeger, Niklas Schülert, Cornelia Dorner-Ciossek, Holger Rosenbrock, and Volker Mack. "M181. DEVELOPMENTAL PROGRESSION OF INTERNEURON NETWORK DEFICITS IN A 15Q13.3 MICRODELETION MOUSE MODEL – A GLIMPSE ON ADOLESCENT PRIMING FOR SCHIZOPHRENIA?" Schizophrenia Bulletin 46, Supplement_1 (2020): S205. http://dx.doi.org/10.1093/schbul/sbaa030.493.

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Abstract Background Schizophrenia is a complex neurodevelopmental disorder. Patients typically start exhibiting symptoms during adolescence, coinciding with a critical period for the maturation of the prefrontal cortex. While previous studies have identified deficits in cortical interneuron integrity and network function in chronic patients, little is known about the maladaptive circuitry in the early prodromal phase of the disease. To assess pathophysiological changes during adolescence that might contribute to the disruption of cortical network function we have studied a 15q13.3 microdeletio

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Benardo, Larry S. "Gabaergic Interneuron Reorganization during the Late Period May Contribute to Hippocampal Epileptogenesis." Epilepsy Currents 2, no. 1 (2002): 28–29. http://dx.doi.org/10.1111/j.1535-7597.2002.00011.x.

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Alterations of Hippocampal GABAergic System Contribute to Development of Spontaneous Recurrent Seizures in the Rat Lithium-Pilocarpine Model of Temporal Lobe Epilepsys Andre V, Marescaux C, Nehlig A, Fritschy JM Hippocampus 2001;11:452–468 Reorganization of excitatory and inhibitory circuits in the hippocampal formation following seizure-induced neuronal loss has been proposed to underlie the development of chronic seizures in temporal lobe epilepsy (TLE). Here, we investigated whether specific morphological alterations of the GABAergic system can be related to the onset of spontaneous recurre

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MacMullin, Paul, Nathaniel Hodgson, Ugur Damar, et al. "Increase in Seizure Susceptibility After Repetitive Concussion Results from Oxidative Stress, Parvalbumin-Positive Interneuron Dysfunction and Biphasic Increases in Glutamate/GABA Ratio." Cerebral Cortex 30, no. 12 (2020): 6108–20. http://dx.doi.org/10.1093/cercor/bhaa157.

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Abstract Chronic symptoms indicating excess cortical excitability follow mild traumatic brain injury, particularly repetitive mild traumatic brain injury (rmTBI). Yet mechanisms underlying post-traumatic excitation/inhibition (E/I) ratio abnormalities may differ between the early and late post-traumatic phases. We therefore measured seizure threshold and cortical gamma-aminobutyric acid (GABA) and glutamate (Glu) concentrations, 1 and 6 weeks after rmTBI in mice. We also analyzed the structure of parvalbumin-positive interneurons (PVIs), their perineuronal nets (PNNs), and their electroencepha

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Kelemen, Krisztina, Károly Orbán-Kis, Ádám Szentes, et al. "Distribution of NECAB1-Positive Neurons in Normal and Epileptic Brain—Expression Changes in Temporal Lobe Epilepsy and Modulation by Levetiracetam and Brivaracetam." International Journal of Molecular Sciences 26, no. 10 (2025): 4906. https://doi.org/10.3390/ijms26104906.

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Calcium-binding proteins (CaBPs) are known to modulate neuronal excitability and calcium signaling, and they may play a role in the imbalances of excitation and inhibition of temporal lobe epilepsy (TLE). While parvalbumin and calretinin are well-characterized CaBPs, N-Terminal EF-Hand Calcium-Binding Protein 1 (NECAB1) remains understudied in epilepsy, despite its association with neurodegenerative conditions. In this study, we used fluorescent immunolabeling to determine the distribution of NECAB1, as well as its co-expression with parvalbumin and calretinin, in brain regions associated with

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Li Volti, Giovanni, Agata Zappalà, Gian Marco Leggio, et al. "Tin chloride enhances parvalbumin-positive interneuron survival by modulating heme metabolism in a model of cerebral ischemia." Neuroscience Letters 492, no. 1 (2011): 33–38. http://dx.doi.org/10.1016/j.neulet.2011.01.048.

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Huang, Ming-Xiong, Charles W. Huang, Deborah L. Harrington, et al. "Marked Increases in Resting-State MEG Gamma-Band Activity in Combat-Related Mild Traumatic Brain Injury." Cerebral Cortex 30, no. 1 (2019): 283–95. http://dx.doi.org/10.1093/cercor/bhz087.

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Abstract Combat-related mild traumatic brain injury (mTBI) is a leading cause of sustained impairments in military service members and veterans. Recent animal studies show that GABA-ergic parvalbumin-positive interneurons are susceptible to brain injury, with damage causing abnormal increases in spontaneous gamma-band (30–80 Hz) activity. We investigated spontaneous gamma activity in individuals with mTBI using high-resolution resting-state magnetoencephalography source imaging. Participants included 25 symptomatic individuals with chronic combat-related blast mTBI and 35 healthy controls with

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Shin, Hyun Seung, Soo Min Choi, Seung Hyun Lee, Ha Jung Moon, and Eui-Man Jung. "A Novel Early Life Stress Model Affects Brain Development and Behavior in Mice." International Journal of Molecular Sciences 24, no. 5 (2023): 4688. http://dx.doi.org/10.3390/ijms24054688.

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Early life stress (ELS) in developing children has been linked to physical and psychological sequelae in adulthood. In the present study, we investigated the effects of ELS on brain and behavioral development by establishing a novel ELS model that combined the maternal separation paradigm and mesh platform condition. We found that the novel ELS model caused anxiety- and depression-like behaviors and induced social deficits and memory impairment in the offspring of mice. In particular, the novel ELS model induced more enhanced depression-like behavior and memory impairment than the maternal sep

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Wang, Weihua, Alexander K. Zinsmaier, Ethan Firestone, et al. "Blocking Tumor Necrosis Factor-Alpha Expression Prevents Blast-Induced Excitatory/Inhibitory Synaptic Imbalance and Parvalbumin-Positive Interneuron Loss in the Hippocampus." Journal of Neurotrauma 35, no. 19 (2018): 2306–16. http://dx.doi.org/10.1089/neu.2018.5688.

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Černotová, Daniela, Karolína Hrůzová, Jan Touš, et al. "Early social deficits in TgF344-AD rats are accompanied by sex-specific parvalbumin-positive interneuron reduction and altered brain oscillations in the hippocampal CA2." Neurobiology of Disease 208 (May 2025): 106875. https://doi.org/10.1016/j.nbd.2025.106875.

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Tada, Mariko, Kenji Kirihara, Yohei Ishishita, et al. "Global and Parallel Cortical Processing Based on Auditory Gamma Oscillatory Responses in Humans." Cerebral Cortex 31, no. 10 (2021): 4518–32. http://dx.doi.org/10.1093/cercor/bhab103.

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Abstract Gamma oscillations are physiological phenomena that reflect perception and cognition, and involve parvalbumin-positive γ-aminobutyric acid-ergic interneuron function. The auditory steady-state response (ASSR) is the most robust index for gamma oscillations, and it is impaired in patients with neuropsychiatric disorders such as schizophrenia and autism. Although ASSR reduction is known to vary in terms of frequency and time, the neural mechanisms are poorly understood. We obtained high-density electrocorticography recordings from a wide area of the cortex in 8 patients with refractory

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Li Volti, Giovanni, Agata Zappalà, Gian Marco Leggio, et al. "Corrigendum to “Tin chloride enhances parvalbumin-positive interneuron survival by modulating heme metabolism in a model of cerebral ischemia” [Neurosci. Lett. 492(1) (2011) 33–38]." Neuroscience Letters 808 (June 2023): 137240. http://dx.doi.org/10.1016/j.neulet.2023.137240.

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Rallapalle, Vyshnavi, Annesha C. King, and Michelle Gray. "BACHD Mice Recapitulate the Striatal Parvalbuminergic Interneuron Loss Found in Huntington’s Disease." Frontiers in Neuroanatomy 15 (May 24, 2021). http://dx.doi.org/10.3389/fnana.2021.673177.

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Huntington’s disease (HD) is a dominantly inherited, adult-onset neurodegenerative disease characterized by motor, psychiatric, and cognitive abnormalities. Neurodegeneration is prominently observed in the striatum where GABAergic medium spiny neurons (MSN) are the most affected neuronal population. Interestingly, recent reports of pathological changes in HD patient striatal tissue have identified a significant reduction in the number of parvalbumin-expressing interneurons which becomes more robust in tissues of higher disease grade. Analysis of other interneuron populations, including somatos

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Mueller-Buehl, Cornelius, Jacqueline Reinhard, Lars Roll, Verian Bader, Konstanze F. Winklhofer, and Andreas Faissner. "Brevican, Neurocan, Tenascin-C, and Tenascin-R Act as Important Regulators of the Interplay Between Perineuronal Nets, Synaptic Integrity, Inhibitory Interneurons, and Otx2." Frontiers in Cell and Developmental Biology 10 (June 2, 2022). http://dx.doi.org/10.3389/fcell.2022.886527.

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Fast-spiking parvalbumin interneurons are critical for the function of mature cortical inhibitory circuits. Most of these neurons are enwrapped by a specialized extracellular matrix (ECM) structure called perineuronal net (PNN), which can regulate their synaptic input. In this study, we investigated the relationship between PNNs, parvalbumin interneurons, and synaptic distribution on these cells in the adult primary visual cortex (V1) of quadruple knockout mice deficient for the ECM molecules brevican, neurocan, tenascin-C, and tenascin-R. We used super-resolution structured illumination micro

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Hamad, Mohammad I. K., Petya Petrova, Solieman Daoud, et al. "Reelin restricts dendritic growth of interneurons in the neocortex." Development 148, no. 17 (2021). http://dx.doi.org/10.1242/dev.199718.

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ABSTRACT Reelin is a large secreted glycoprotein that regulates neuronal migration, lamination and establishment of dendritic architecture in the embryonic brain. Reelin expression switches postnatally from Cajal-Retzius cells to interneurons. However, reelin function in interneuron development is still poorly understood. Here, we have investigated the role of reelin in interneuron development in the postnatal neocortex. To preclude early cortical migration defects caused by reelin deficiency, we employed a conditional reelin knockout (RelncKO) mouse to induce postnatal reelin deficiency. Indu

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Yu, Diankun, Tao Li, Jean-Christophe Delpech, et al. "Microglial GPR56 is the molecular target of maternal immune activation-induced parvalbumin-positive interneuron deficits." Science Advances 8, no. 18 (2022). http://dx.doi.org/10.1126/sciadv.abm2545.

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Parvalbumin-positive (PV + ) interneurons play a critical role in maintaining circuit rhythm in the brain, and their reduction is implicated in autism spectrum disorders. Animal studies demonstrate that maternal immune activation (MIA) leads to reduced PV + interneurons in the somatosensory cortex and autism-like behaviors. However, the underlying molecular mechanisms remain largely unknown. Here, we show that MIA down-regulates microglial Gpr56 expression in fetal brains in an interleukin-17a–dependent manner and that conditional deletion of microglial Gpr56 [ Gpr56 conditional knockout (cKO)

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Wang, Siyan, Cristen Kfoury, Alexis Marion, Maxime Lévesque, and Massimo Avoli. "Modulation of in vitro epileptiform activity by optogenetic stimulation of parvalbumin-positive interneurons." Journal of Neurophysiology, August 31, 2022. http://dx.doi.org/10.1152/jn.00192.2022.

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GABAA signaling is surprisingly involved in the initiation of epileptiform activity since increased interneuron firing, presumably leading to excessive GABA release, often precedes ictal discharges. Field potential theta (4-12 Hz) oscillations, which are thought to mirror the synchronization of interneuron networks, also lead to ictogenesis. However, the exact role of parvalbumin-positive (PV) interneurons in generating theta oscillations linked to epileptiform discharges remains unexplored. We analyzed here the field responses recorded in the CA3, entorhinal cortex (EC) and dentate gyrus (DG)

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Kuhl, Lydia M., Matthew S. Jeffers, Nicolay Hristozov, et al. "Post-Stroke Recovery in Relation to Parvalbumin-Positive Interneurons and Perineuronal Nets." Neurorehabilitation and Neural Repair, January 16, 2025. https://doi.org/10.1177/15459683241309567.

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Background: There is a critical time window of post-stroke neuroplasticity when spontaneous behavioral recovery occurs. Potential factors responsible for this heightened plasticity are the reduction of parvalbumin-immunoreactive (PV+) interneuron inhibitory signaling and the disappearance of extracellular matrix synaptic stabilizers called perineuronal net(s; PNN/PNNs). Objective: This study investigated whether behavioral recovery during this critical period following stroke is associated with changes in densities of PV+ interneurons and PNNs. Methods Male, Sprague-Dawley rats received foreli

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Gothner, Tina, Pedro J. Gonçalves, Maneesh Sahani, Jennifer F. Linden, and K. Jannis Hildebrandt. "Sustained Activation of PV+ Interneurons in Core Auditory Cortex Enables Robust Divisive Gain Control for Complex and Naturalistic Stimuli." Cerebral Cortex, December 10, 2020. http://dx.doi.org/10.1093/cercor/bhaa347.

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Abstract Sensory cortices must flexibly adapt their operations to internal states and external requirements. Sustained modulation of activity levels in different inhibitory interneuron populations may provide network-level mechanisms for adjustment of sensory cortical processing on behaviorally relevant timescales. However, understanding of the computational roles of inhibitory interneuron modulation has mostly been restricted to effects at short timescales, through the use of phasic optogenetic activation and transient stimuli. Here, we investigated how modulation of inhibitory interneurons a

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Stedehouder, Jeffrey, Demi Brizee, Johan A. Slotman, et al. "Local axonal morphology guides the topography of interneuron myelination in mouse and human neocortex." eLife 8 (November 19, 2019). http://dx.doi.org/10.7554/elife.48615.

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GABAergic fast-spiking parvalbumin-positive (PV) interneurons are frequently myelinated in the cerebral cortex. However, the factors governing the topography of cortical interneuron myelination remain incompletely understood. Here, we report that segmental myelination along neocortical interneuron axons is strongly predicted by the joint combination of interbranch distance and local axon caliber. Enlargement of PV+ interneurons increased axonal myelination, while reduced cell size led to decreased myelination. Next, we considered regular-spiking SOM+ cells, which normally have relatively short

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Göngrich, Christina, Favio A. Krapacher, Hermany Munguba, et al. "ALK4 coordinates extracellular and intrinsic signals to regulate development of cortical somatostatin interneurons." Journal of Cell Biology 219, no. 1 (2019). http://dx.doi.org/10.1083/jcb.201905002.

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Although the role of transcription factors in fate specification of cortical interneurons is well established, how these interact with extracellular signals to regulate interneuron development is poorly understood. Here we show that the activin receptor ALK4 is a key regulator of the specification of somatostatin interneurons. Mice lacking ALK4 in GABAergic neurons of the medial ganglionic eminence (MGE) showed marked deficits in distinct subpopulations of somatostatin interneurons from early postnatal stages of cortical development. Specific losses were observed among distinct subtypes of som

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Zucca, Stefano, Giulia D'Urso, Valentina Pasquale, et al. "An inhibitory gate for state transition in cortex." eLife, May 16, 2017. https://doi.org/10.7554/eLife.26177.

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Large scale transitions between active (up) and silent (down) states during quiet wakefulness or NREM sleep regulate fundamental cortical functions and are known to involve both excitatory and inhibitory cells. However, if and how inhibition regulates these activity transitions is unclear. Using fluorescence-targeted electrophysiological recording and cell-specific optogenetic manipulation in both anesthetized and non-anesthetized mice, we found that two major classes of interneurons, the parvalbumin and the somatostatin positive cells, tightly control both up-to-down and down-to-up state tran

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Hainmueller, Thomas, Aurore Cazala, Li-Wen Huang, and Marlene Bartos. "Subfield-specific interneuron circuits govern the hippocampal response to novelty in male mice." Nature Communications 15, no. 1 (2024). http://dx.doi.org/10.1038/s41467-024-44882-3.

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AbstractThe hippocampus is the brain’s center for episodic memories. Its subregions, the dentate gyrus and CA1-3, are differentially involved in memory encoding and recall. Hippocampal principal cells represent episodic features like movement, space, and context, but less is known about GABAergic interneurons. Here, we performed two-photon calcium imaging of parvalbumin- and somatostatin-expressing interneurons in the dentate gyrus and CA1-3 of male mice exploring virtual environments. Parvalbumin-interneurons increased activity with running-speed and reduced it in novel environments. Somatost

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Godoy, Lívea Dornela, Tamiris Prizon, Matheus Teixeira Rossignoli, João Pereira Leite, and José Luiz Liberato. "Parvalbumin Role in Epilepsy and Psychiatric Comorbidities: From Mechanism to Intervention." Frontiers in Integrative Neuroscience 16 (February 17, 2022). http://dx.doi.org/10.3389/fnint.2022.765324.

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Parvalbumin is a calcium-binding protein present in inhibitory interneurons that play an essential role in regulating many physiological processes, such as intracellular signaling and synaptic transmission. Changes in parvalbumin expression are deeply related to epilepsy, which is considered one of the most disabling neuropathologies. Epilepsy is a complex multi-factor group of disorders characterized by periods of hypersynchronous activity and hyperexcitability within brain networks. In this scenario, inhibitory neurotransmission dysfunction in modulating excitatory transmission related to th

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Tessier, Marine, Marta Saez Garcia, Emmanuelle Goubert, et al. "Bumetanide induces post-traumatic microglia–interneuron contact to promote neurogenesis and recovery." Brain, April 21, 2023. http://dx.doi.org/10.1093/brain/awad132.

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Abstract Although the Na-K-Cl cotransporter (NKCC1) inhibitor bumetanide has prominent positive effects on the pathophysiology of many neurological disorders, the mechanism of action is obscure. Attention for elucidating the role of Nkcc1 has been mainly focused on neurons. Recent single cell mRNA sequencing analysis has demonstrated that the major cellular populations expressing NKCC1 in the cortex are non-neuronal. We used a combination of conditional transgenic animals, in vivo electrophysiology, two-photon imaging, cognitive behavioral tests and flow cytometry to investigate the role of Nk

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Shen, Kaiyuan, Yandong Zhang, Yunyun Huang, Yunli Xie, Jing Ding, and Xin Wang. "Prenatal Valproic Acid Exposure Impairs Offspring Cognition Through Disturbing Interneuron Development." CNS Neuroscience & Therapeutics 31, no. 2 (2025). https://doi.org/10.1111/cns.70303.

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ABSTRACTAimsValproic acid (VPA) exposure during the gestational period has been found to impair the cognition of the offspring. The study aimed to investigate whether VPA leads to offspring cognitive impairment through disturbing interneuron development.MethodsPregnant mice were injected with VPA peritoneally to establish the prenatal VPA exposure model. Cortical interneurons were labeled with Rosa26‐EYFP/− reporter mice activated by Nkx2.1‐Cre. Interneuron subtypes both in the cortex and the hippocampus were detected by immunofluorescence. A battery of behavioral tests was conducted on postna

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Umbricht, Daniel. "Matrix metalloproteinase 9 levels and parvalbumin positive interneuron dysfunction." Neuropsychopharmacology, June 7, 2021. http://dx.doi.org/10.1038/s41386-021-01048-9.

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Wyroślak, Marcin, Grzegorz Dobrzański, and Jerzy W. Mozrzymas. "Bidirectional plasticity of GABAergic tonic inhibition in hippocampal somatostatin- and parvalbumin-containing interneurons." Frontiers in Cellular Neuroscience 17 (June 28, 2023). http://dx.doi.org/10.3389/fncel.2023.1193383.

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GABAA receptors present in extrasynaptic areas mediate tonic inhibition in hippocampal neurons regulating the performance of neural networks. In this study, we investigated the effect of NMDA-induced plasticity on tonic inhibition in somatostatin- and parvalbumin-containing interneurons. Using pharmacological methods and transgenic mice (SST-Cre/PV-Cre x Ai14), we induced the plasticity of GABAergic transmission in somatostatin- and parvalbumin-containing interneurons by a brief (3 min) application of NMDA. In the whole-cell patch-clamp configuration, we measured tonic currents enhanced by spe

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Dufour, Brett D., Erin McBride, Trevor Bartley, Pablo Juarez, and Verónica Martínez-Cerdeño. "Distinct patterns of GABAergic interneuron pathology in autism are associated with intellectual impairment and stereotypic behaviors." Autism, March 19, 2023, 136236132311540. http://dx.doi.org/10.1177/13623613231154053.

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Autism spectrum disorder is a neurodevelopmental condition characterized by deficits in social communication and repetitive behaviors. How specific anatomical alterations contribute to the clinical profile of autism spectrum disorder remains largely uncharacterized. We have previously shown that parvalbumin-positive Chandelier cells, a specific type of GABAergic interneuron, are reduced in number in the autism spectrum disorder prefrontal cortex. Here, we assessed the relationship between interneuron pathology with autism spectrum disorder symptom severity and comorbidity. We collected clinica

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Voelkl, Kerstin, Elena Katharina Schulz-Trieglaff, Rüdiger Klein, and Irina Dudanova. "Distinct histological alterations of cortical interneuron types in mouse models of Huntington’s disease." Frontiers in Neuroscience 16 (September 26, 2022). http://dx.doi.org/10.3389/fnins.2022.1022251.

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Huntington’s disease (HD) is a debilitating hereditary motor disorder caused by an expansion of the CAG triplet repeat in the Huntingtin gene. HD causes neurodegeneration particularly in the basal ganglia and neocortex. In the cortex, glutamatergic pyramidal neurons are known to be severely affected by the disease, but the involvement of GABAergic interneurons remains unclear. Here, we use a combination of immunostaining and genetic tracing to investigate histological changes in three major cortical interneuron types — parvalbumin (PV), somatostatin (SST), and vasoactive intestinal peptide (VI

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Jézéquel, Julie, Giuseppe Condomitti, Tim Kroon, et al. "Cadherins orchestrate specific patterns of perisomatic inhibition onto distinct pyramidal cell populations." Nature Communications 16, no. 1 (2025). https://doi.org/10.1038/s41467-025-59635-z.

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Abstract GABAergic interneurons were thought to regulate excitatory networks by establishing unselective connections onto diverse pyramidal cell populations, but recent studies demonstrate the existence of a cell type-specific inhibitory connectome. How and when interneurons establish precise connectivity patterns among intermingled populations of excitatory neurons remains enigmatic. We explore the molecular mechanisms orchestrating the emergence of cell type-specific inhibition in the mouse cerebral cortex. We demonstrate that layer 5 intra- (L5 IT) and extra-telencephalic (L5 ET) neurons ex

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