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1

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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2

Riedemann, Therese. "Diversity and Function of Somatostatin-Expressing Interneurons in the Cerebral Cortex." International Journal of Molecular Sciences 20, no. 12 (2019): 2952. http://dx.doi.org/10.3390/ijms20122952.

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Inhibitory interneurons make up around 10–20% of the total neuron population in the cerebral cortex. A hallmark of inhibitory interneurons is their remarkable diversity in terms of morphology, synaptic connectivity, electrophysiological and neurochemical properties. It is generally understood that there are three distinct and non-overlapping interneuron classes in the mouse neocortex, namely, parvalbumin-expressing, 5-HT3A receptor-expressing and somatostatin-expressing interneuron classes. Each class is, in turn, composed of a multitude of subclasses, resulting in a growing number of interneu
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3

Lukomska, Agnieszka, Grzegorz Dobrzanski, Monika Liguz-Lecznar, and Malgorzata Kossut. "Somatostatin receptors (SSTR1-5) on inhibitory interneurons in the barrel cortex." Brain Structure and Function 225, no. 1 (2019): 387–401. http://dx.doi.org/10.1007/s00429-019-02011-7.

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AbstractInhibitory interneurons in the cerebral cortex contain specific proteins or peptides characteristic for a certain interneuron subtype. In mice, three biochemical markers constitute non-overlapping interneuron populations, which account for 80–90% of all inhibitory cells. These interneurons express parvalbumin (PV), somatostatin (SST), or vasoactive intestinal peptide (VIP). SST is not only a marker of a specific interneuron subtype, but also an important neuropeptide that participates in numerous biochemical and signalling pathways in the brain via somatostatin receptors (SSTR1-5). In
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4

Friend, Lindsey, Ryan Williamson, Collin Merrill, et al. "Hippocampal Stratum Oriens Somatostatin-Positive Cells Undergo CB1-Dependent Long-Term Potentiation and Express Endocannabinoid Biosynthetic Enzymes." Molecules 24, no. 7 (2019): 1306. http://dx.doi.org/10.3390/molecules24071306.

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The hippocampus is thought to encode information by altering synaptic strength via synaptic plasticity. Some forms of synaptic plasticity are induced by lipid-based endocannabinoid signaling molecules that act on cannabinoid receptors (CB1). Endocannabinoids modulate synaptic plasticity of hippocampal pyramidal cells and stratum radiatum interneurons; however, the role of endocannabinoids in mediating synaptic plasticity of stratum oriens interneurons is unclear. These feedback inhibitory interneurons exhibit presynaptic long-term potentiation (LTP), but the exact mechanism is not entirely und
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5

Henriques, Vanessa Jorge, Angela Chiavegato, Giorgio Carmignoto, and Marta Gómez-Gonzalo. "Astrocytes Modulate Somatostatin Interneuron Signaling in the Visual Cortex." Cells 11, no. 9 (2022): 1400. http://dx.doi.org/10.3390/cells11091400.

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At glutamatergic synapses, astrocytes respond to the neurotransmitter glutamate with intracellular Ca2+ elevations and the release of gliotransmitters that modulate synaptic transmission. While the functional interactions between neurons and astrocytes have been intensively studied at glutamatergic synapses, the role of astrocytes at GABAergic synapses has been less investigated. In the present study, we combine optogenetics with 2-photon Ca2+ imaging experiments and patch-clamp recording techniques to investigate the signaling between Somatostatin (SST)-releasing GABAergic interneurons and as
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6

Halabisky, Brian, Fran Shen, John R. Huguenard, and David A. Prince. "Electrophysiological Classification of Somatostatin-Positive Interneurons in Mouse Sensorimotor Cortex." Journal of Neurophysiology 96, no. 2 (2006): 834–45. http://dx.doi.org/10.1152/jn.01079.2005.

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Classification of inhibitory interneurons is critical in determining their role in normal information processing and pathophysiological conditions such as epilepsy. Classification schemes have relied on morphological, physiological, biochemical, and molecular criteria; and clear correlations have been demonstrated between firing patterns and cellular markers such as neuropeptides and calcium-binding proteins. This molecular diversity has allowed generation of transgenic mouse strains in which GFP expression is linked to the expression of one of these markers and presumably a single subtype of
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7

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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8

Vaes, Josine E. G., Chantal M. Kosmeijer, Marthe Kaal, et al. "Regenerative Therapies to Restore Interneuron Disturbances in Experimental Models of Encephalopathy of Prematurity." International Journal of Molecular Sciences 22, no. 1 (2020): 211. http://dx.doi.org/10.3390/ijms22010211.

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Encephalopathy of Prematurity (EoP) is a major cause of morbidity in (extreme) preterm neonates. Though the majority of EoP research has focused on failure of oligodendrocyte maturation as an underlying pathophysiological mechanism, recent pioneer work has identified developmental disturbances in inhibitory interneurons to contribute to EoP. Here we investigated interneuron abnormalities in two experimental models of EoP and explored the potential of two promising treatment strategies, namely intranasal mesenchymal stem cells (MSCs) or insulin-like growth factor I (IGF1), to restore interneuro
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9

De Gregorio, Roberto, Xiaoning Chen, Emilie I. Petit, Kostantin Dobrenis, and Ji Ying Sze. "Disruption of Transient SERT Expression in Thalamic Glutamatergic Neurons Alters Trajectory of Postnatal Interneuron Development in the Mouse Cortex." Cerebral Cortex 30, no. 3 (2019): 1623–36. http://dx.doi.org/10.1093/cercor/bhz191.

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Abstract In mice, terminal differentiation of subpopulations of interneurons occurs in late postnatal stages, paralleling the emergence of the adult cortical architecture. Here, we investigated the effects of altered initial cortical architecture on later interneuron development. We identified that a class of somatostatin (SOM)-expressing GABAergic interneurons undergoes terminal differentiation between 2nd and 3rd postnatal week in the mouse somatosensory barrel cortex and upregulates Reelin expression during neurite outgrowth. Our previous work demonstrated that transient expression (E15-P10
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10

Shen, Wei, Ru Ba, Yan Su, et al. "Foxg1 Regulates the Postnatal Development of Cortical Interneurons." Cerebral Cortex 29, no. 4 (2018): 1547–60. http://dx.doi.org/10.1093/cercor/bhy051.

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AbstractAbnormalities in cortical interneurons are closely associated with neurological diseases. Most patients with Foxg1 syndrome experience seizures, suggesting a possible role of Foxg1 in the cortical interneuron development. Here, by conditional deletion of Foxg1, which was achieved by crossing Foxg1fl/fl with the Gad2-CreER line, we found the postnatal distributions of somatostatin-, calretinin-, and neuropeptide Y-positive interneurons in the cortex were impaired. Further investigations revealed an enhanced dendritic complexity and decreased migration capacity of Foxg1-deficient interne
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11

Large, Adam M., Nathan W. Vogler, Martha Canto-Bustos, F. Kathryn Friason, Paul Schick, and Anne-Marie M. Oswald. "Differential inhibition of pyramidal cells and inhibitory interneurons along the rostrocaudal axis of anterior piriform cortex." Proceedings of the National Academy of Sciences 115, no. 34 (2018): E8067—E8076. http://dx.doi.org/10.1073/pnas.1802428115.

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The spatial representation of stimuli in sensory neocortices provides a scaffold for elucidating circuit mechanisms underlying sensory processing. However, the anterior piriform cortex (APC) lacks topology for odor identity as well as afferent and intracortical excitation. Consequently, olfactory processing is considered homogenous along the APC rostral–caudal (RC) axis. We recorded excitatory and inhibitory neurons in APC while optogenetically activating GABAergic interneurons along the RC axis. In contrast to excitation, we find opposing, spatially asymmetric inhibition onto pyramidal cells
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12

Lee, L., L. Boorman, E. Glendenning, et al. "Key Aspects of Neurovascular Control Mediated by Specific Populations of Inhibitory Cortical Interneurons." Cerebral Cortex 30, no. 4 (2019): 2452–64. http://dx.doi.org/10.1093/cercor/bhz251.

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Abstract Inhibitory interneurons can evoke vasodilation and vasoconstriction, making them potential cellular drivers of neurovascular coupling. However, the specific regulatory roles played by particular interneuron subpopulations remain unclear. Our purpose was therefore to adopt a cell-specific optogenetic approach to investigate how somatostatin (SST) and neuronal nitric oxide synthase (nNOS)-expressing interneurons might influence the neurovascular relationship. In mice, specific activation of SST- or nNOS-interneurons was sufficient to evoke hemodynamic changes. In the case of nNOS-intern
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13

ter Wal, Marije, and Paul H. E. Tiesinga. "Comprehensive characterization of oscillatory signatures in a model circuit with PV- and SOM-expressing interneurons." Biological Cybernetics 115, no. 5 (2021): 487–517. http://dx.doi.org/10.1007/s00422-021-00894-6.

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AbstractNeural circuits contain a wide variety of interneuron types, which differ in their biophysical properties and connectivity patterns. The two most common interneuron types, parvalbumin-expressing and somatostatin-expressing cells, have been shown to be differentially involved in many cognitive functions. These cell types also show different relationships with the power and phase of oscillations in local field potentials. The mechanisms that underlie the emergence of different oscillatory rhythms in neural circuits with more than one interneuron subtype, and the roles specific interneuro
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14

Provenzano, Giovanni, Angela Gilardoni, Marika Maggia, et al. "Altered Expression of GABAergic Markers in the Forebrain of Young and Adult Engrailed-2 Knockout Mice." Genes 11, no. 4 (2020): 384. http://dx.doi.org/10.3390/genes11040384.

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Impaired function of GABAergic interneurons, and the subsequent alteration of excitation/inhibition balance, is thought to contribute to autism spectrum disorders (ASD). Altered numbers of GABAergic interneurons and reduced expression of GABA receptors has been detected in the brain of ASD subjects and mouse models of ASD. We previously showed a reduced expression of GABAergic interneuron markers parvalbumin (PV) and somatostatin (SST) in the forebrain of adult mice lacking the Engrailed2 gene (En2-/- mice). Here, we extended this analysis to postnatal day (P) 30 by using in situ hybridization
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15

Hu, Hang, and Ariel Agmon. "Properties of precise firing synchrony between synaptically coupled cortical interneurons depend on their mode of coupling." Journal of Neurophysiology 114, no. 1 (2015): 624–37. http://dx.doi.org/10.1152/jn.00304.2015.

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Precise spike synchrony has been widely reported in the central nervous system, but its functional role in encoding, processing, and transmitting information is yet unresolved. Of particular interest is firing synchrony between inhibitory cortical interneurons, thought to drive various cortical rhythms such as gamma oscillations, the hallmark of cognitive states. Precise synchrony can arise between two interneurons connected electrically, through gap junctions, chemically, through fast inhibitory synapses, or dually, through both types of connections, but the properties of synchrony generated
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16

Keijser, Joram, and Henning Sprekeler. "Optimizing interneuron circuits for compartment-specific feedback inhibition." PLOS Computational Biology 18, no. 4 (2022): e1009933. http://dx.doi.org/10.1371/journal.pcbi.1009933.

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Cortical circuits process information by rich recurrent interactions between excitatory neurons and inhibitory interneurons. One of the prime functions of interneurons is to stabilize the circuit by feedback inhibition, but the level of specificity on which inhibitory feedback operates is not fully resolved. We hypothesized that inhibitory circuits could enable separate feedback control loops for different synaptic input streams, by means of specific feedback inhibition to different neuronal compartments. To investigate this hypothesis, we adopted an optimization approach. Leveraging recent ad
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17

Mazza, Frank, Alexandre Guet-McCreight, Taufik A. Valiante, John D. Griffiths, and Etay Hay. "In-silico EEG biomarkers of reduced inhibition in human cortical microcircuits in depression." PLOS Computational Biology 19, no. 4 (2023): e1010986. http://dx.doi.org/10.1371/journal.pcbi.1010986.

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Reduced cortical inhibition by somatostatin-expressing (SST) interneurons has been strongly associated with treatment-resistant depression. However, due to technical limitations it is impossible to establish experimentally in humans whether the effects of reduced SST interneuron inhibition on microcircuit activity have signatures detectable in clinically-relevant brain signals such as electroencephalography (EEG). To overcome these limitations, we simulated resting-state activity and EEG using detailed models of human cortical microcircuits with normal (healthy) or reduced SST interneuron inhi
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18

Bryson, Alexander, Robert John Hatch, Bas-Jan Zandt, et al. "GABA-mediated tonic inhibition differentially modulates gain in functional subtypes of cortical interneurons." Proceedings of the National Academy of Sciences 117, no. 6 (2020): 3192–202. http://dx.doi.org/10.1073/pnas.1906369117.

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The binding of GABA (γ-aminobutyric acid) to extrasynaptic GABAA receptors generates tonic inhibition that acts as a powerful modulator of cortical network activity. Despite GABA being present throughout the extracellular space of the brain, previous work has shown that GABA may differentially modulate the excitability of neuron subtypes according to variation in chloride gradient. Here, using biophysically detailed neuron models, we predict that tonic inhibition can differentially modulate the excitability of neuron subtypes according to variation in electrophysiological properties. Surprisin
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Novák, Ondřej, Ondřej Zelenka, Tomáš Hromádka, and Josef Syka. "Immediate manifestation of acoustic trauma in the auditory cortex is layer specific and cell type dependent." Journal of Neurophysiology 115, no. 4 (2016): 1860–74. http://dx.doi.org/10.1152/jn.00810.2015.

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Exposure to loud sounds damages the auditory periphery and induces maladaptive changes in central parts of the auditory system. Diminished peripheral afferentation and altered inhibition influence the processing of sounds in the auditory cortex. It is unclear, however, which types of inhibitory interneurons are affected by acoustic trauma. Here we used single-unit electrophysiological recording and two-photon calcium imaging in anesthetized mice to evaluate the effects of acute acoustic trauma (125 dB SPL, white noise, 5 min) on the response properties of neurons in the core auditory cortex. E
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Litwin-Kumar, Ashok, Robert Rosenbaum, and Brent Doiron. "Inhibitory stabilization and visual coding in cortical circuits with multiple interneuron subtypes." Journal of Neurophysiology 115, no. 3 (2016): 1399–409. http://dx.doi.org/10.1152/jn.00732.2015.

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Recent anatomical and functional characterization of cortical inhibitory interneurons has highlighted the diverse computations supported by different subtypes of interneurons. However, most theoretical models of cortex do not feature multiple classes of interneurons and rather assume a single homogeneous population. We study the dynamics of recurrent excitatory-inhibitory model cortical networks with parvalbumin (PV)-, somatostatin (SOM)-, and vasointestinal peptide-expressing (VIP) interneurons, with connectivity properties motivated by experimental recordings from mouse primary visual cortex
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Halabisky, Brian, Isabel Parada, Paul S. Buckmaster, and David A. Prince. "Excitatory Input Onto Hilar Somatostatin Interneurons Is Increased in a Chronic Model of Epilepsy." Journal of Neurophysiology 104, no. 4 (2010): 2214–23. http://dx.doi.org/10.1152/jn.00147.2010.

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The density of somatostatin (SOM)-containing GABAergic interneurons in the hilus of the dentate gyrus is significantly decreased in both human and experimental temporal lobe epilepsy. We used the pilocarpine model of status epilepticus and temporal lobe epilepsy in mice to study anatomical and electrophysiological properties of surviving somatostatin interneurons and determine whether compensatory functional changes occur that might offset loss of other inhibitory neurons. Using standard patch-clamp techniques and pipettes containing biocytin, whole cell recordings were obtained in hippocampal
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Grider, J. R. "Regulation of excitatory neural input to longitudinal intestinal muscle by myenteric interneurons." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 5 (1998): G973—G978. http://dx.doi.org/10.1152/ajpgi.1998.275.5.g973.

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The circuit of myenteric interneurons that regulate excitatory input to longitudinal colonic muscle was identified using dispersed ganglia and longitudinal muscle strips with adherent myenteric plexus from rat distal colon. The preparations enabled measurement of neurotransmitter release from interneurons and/or excitatory motoneurons innervating longitudinal muscle. 1,1-Dimethyl-4-phenylpiperizinium (DMPP) and somatostatin were used to activate myenteric neurons in dispersed ganglia and muscle strips, respectively. DMPP-stimulated vasoactive intestinal peptide (VIP) release in dispersed gangl
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Grider, J. R. "Somatostatin release from isolated ganglia of the myenteric plexus." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 2 (1989): G313—G315. http://dx.doi.org/10.1152/ajpgi.1989.257.2.g313.

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Somatostatin neurons of the myenteric plexus project caudad exclusively within the plexus synapsing with neurons in the same or other ganglia. Isolated ganglia offer a unique opportunity to examine peptide transmitter release from these interneurons. Ganglia were isolated from the myenteric plexus by sequential enzymatic digestion, centrifugation, and filtration. Single ganglia were harvested by suction and dispersed in polyacrylamide gel. The ganglia were placed in chambers (200 ganglia/chamber) and perfused with Krebs medium at the rate of 1 ml/min. Addition of the nicotinic agonist, dimethy
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Boksa, Patricia, Ying Zhang, Dominique Nouel, Alice Wong, and Tak Pan Wong. "Early Development of Parvalbumin-, Somatostatin-, and Cholecystokinin-Expressing Neurons in Rat Brain following Prenatal Immune Activation and Maternal Iron Deficiency." Developmental Neuroscience 38, no. 5 (2016): 342–53. http://dx.doi.org/10.1159/000454677.

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Prenatal maternal infection and maternal iron deficiency during pregnancy are 2 early environmental insults associated with increased risk for schizophrenia in offspring. Substantial evidence suggests that abnormalities in inhibitory γ-aminobutyric acid (GABA) interneuron function, especially in the parvalbumin subtype of GABA interneuron, both developmentally and in adulthood, may contribute mechanistically to cognitive deficits and psychotic symptoms in schizophrenia. This study used a rat model to test whether prenatal immune activation with lipopolysaccharide (LPS; at gestation days, GD, 1
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Horn, Meryl E., and Roger A. Nicoll. "Somatostatin and parvalbumin inhibitory synapses onto hippocampal pyramidal neurons are regulated by distinct mechanisms." Proceedings of the National Academy of Sciences 115, no. 3 (2018): 589–94. http://dx.doi.org/10.1073/pnas.1719523115.

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Excitation–inhibition balance is critical for optimal brain function, yet the mechanisms underlying the tuning of inhibition from different populations of inhibitory neurons are unclear. Here, we found evidence for two distinct pathways through which excitatory neurons cell-autonomously modulate inhibitory synapses. Synapses from parvalbumin-expressing interneurons onto hippocampal pyramidal neurons are regulated by neuronal firing, signaling through L-type calcium channels. Synapses from somatostatin-expressing interneurons are regulated by NMDA receptors, signaling through R-type calcium cha
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Paluszkiewicz, Scott M., Jose Luis Olmos-Serrano, Joshua G. Corbin, and Molly M. Huntsman. "Impaired inhibitory control of cortical synchronization in fragile X syndrome." Journal of Neurophysiology 106, no. 5 (2011): 2264–72. http://dx.doi.org/10.1152/jn.00421.2011.

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Fragile X syndrome (FXS) is a neurodevelopmental disorder characterized by severe cognitive impairments, sensory hypersensitivity, and comorbidities with autism and epilepsy. Fmr1 knockout (KO) mouse models of FXS exhibit alterations in excitatory and inhibitory neurotransmission, but it is largely unknown how aberrant function of specific neuronal subtypes contributes to these deficits. In this study we show specific inhibitory circuit dysfunction in layer II/III of somatosensory cortex of Fmr1 KO mice. We demonstrate reduced activation of somatostatin-expressing low-threshold-spiking (LTS) i
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Delorme, James, Lijing Wang, Femke Roig Kuhn, et al. "Sleep loss drives acetylcholine- and somatostatin interneuron–mediated gating of hippocampal activity to inhibit memory consolidation." Proceedings of the National Academy of Sciences 118, no. 32 (2021): e2019318118. http://dx.doi.org/10.1073/pnas.2019318118.

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Sleep loss disrupts consolidation of hippocampus-dependent memory. To characterize effects of learning and sleep loss, we quantified activity-dependent phosphorylation of ribosomal protein S6 (pS6) across the dorsal hippocampus of mice. We find that pS6 is enhanced in dentate gyrus (DG) following single-trial contextual fear conditioning (CFC) but is reduced throughout the hippocampus after brief sleep deprivation (SD; which disrupts contextual fear memory [CFM] consolidation). To characterize neuronal populations affected by SD, we used translating ribosome affinity purification sequencing to
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Delorme, James, Lijing Wang, Femke Kuhn, et al. "028 Sleep loss disrupts hippocampal memory consolidation via an acetylcholine- and somatostatin interneuron-mediated inhibitory gate." Sleep 44, Supplement_2 (2021): A12—A13. http://dx.doi.org/10.1093/sleep/zsab072.027.

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Abstract Introduction Sleep loss profoundly disrupts consolidation of hippocampus-dependent memory. To better characterize effects of learning and sleep loss on the hippocampal circuit, we quantified activity-dependent phosphorylation of ribosomal subunit S6 (pS6) across the dorsal hippocampus of mice. Methods We first measured pS6 throughout the hippocampus after learning (single trial contextual fear conditioning; CFC), and after subsequent sleep or sleep deprivation (SD). To characterize cell populations with activity affected by SD, we used translating ribosome affinity purification (TRAP)
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Zichó, Krisztián, Katalin E. Sos, Péter Papp, et al. "Fear memory recall involves hippocampal somatostatin interneurons." PLOS Biology 21, no. 6 (2023): e3002154. http://dx.doi.org/10.1371/journal.pbio.3002154.

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Fear-related memory traces are encoded by sparse populations of hippocampal principal neurons that are recruited based on their inhibitory–excitatory balance during memory formation. Later, the reactivation of the same principal neurons can recall the memory. The details of this mechanism are still unclear. Here, we investigated whether disinhibition could play a major role in this process. Using optogenetic behavioral experiments, we found that when fear was associated with the inhibition of mouse hippocampal somatostatin positive interneurons, the re-inhibition of the same interneurons could
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Likhtik, Ekaterina, Joseph Stujenske, Pia-Kelsey O'Neill, et al. "Somatostatin Interneurons in Emotion Regulation." Biological Psychiatry 93, no. 9 (2023): S4. http://dx.doi.org/10.1016/j.biopsych.2023.02.031.

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Banasr, Mounira, Ashley Lepack, Corey Fee, et al. "Characterization of GABAergic Marker Expression in the Chronic Unpredictable Stress Model of Depression." Chronic Stress 1 (February 2017): 247054701772045. http://dx.doi.org/10.1177/2470547017720459.

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Background Evidence continues to build suggesting that the GABAergic neurotransmitter system is altered in brains of patients with major depressive disorder. However, there is little information available related to the extent of these changes or the potential mechanisms associated with these alterations. As stress is a well-established precipitant to depressive episodes, we sought to explore the impact of chronic stress on GABAergic interneurons. Methods Using western blot analyses and quantitative real-time polymerase chain reaction, we assessed the effects of five-weeks of chronic unpredict
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Grider, J. R., A. Arimura, and G. M. Makhlouf. "Role of somatostatin neurons in intestinal peristalsis: facilitatory interneurons in descending pathways." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 4 (1987): G434—G438. http://dx.doi.org/10.1152/ajpgi.1987.253.4.g434.

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The role of somatostatin neurons in the regulation of peristalsis was examined in segments of rat colon that permit separate characterization of the ascending contraction and descending relaxation components of the peristaltic reflex. Release of somatostatin and vasoactive intestinal peptide (VIP) increased significantly only during descending relaxation. Preincubation of the segment with somatostatin antiserum (final concentration 1:40) decreased VIP release and descending relaxation. Addition of somatostatin (1 nM to 1 microM) augmented VIP release and descending relaxation in a concentratio
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Liguz-Lecznar, Monika, Grzegorz Dobrzanski, and Malgorzata Kossut. "Somatostatin and Somatostatin-Containing Interneurons—From Plasticity to Pathology." Biomolecules 12, no. 2 (2022): 312. http://dx.doi.org/10.3390/biom12020312.

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Despite the obvious differences in the pathophysiology of distinct neuropsychiatric diseases or neurodegenerative disorders, some of them share some general but pivotal mechanisms, one of which is the disruption of excitation/inhibition balance. Such an imbalance can be generated by changes in the inhibitory system, very often mediated by somatostatin-containing interneurons (SOM-INs). In physiology, this group of inhibitory interneurons, as well as somatostatin itself, profoundly shapes the brain activity, thus influencing the behavior and plasticity; however, the changes in the number, densi
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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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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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Arriaga, Moises, and Edward B. Han. "Structured inhibitory activity dynamics in new virtual environments." eLife 8 (October 8, 2019). http://dx.doi.org/10.7554/elife.47611.

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Inhibition plays a powerful role in regulating network excitation and plasticity; however, the activity of defined interneuron types during spatial exploration remain poorly understood. Using two-photon calcium imaging, we recorded hippocampal CA1 somatostatin- and parvalbumin-expressing interneurons as mice performed a goal-directed spatial navigation task in new visual virtual reality (VR) contexts. Activity in both interneuron classes was strongly suppressed but recovered as animals learned to adapt the previously learned task to the new spatial context. Surprisingly, although there was a r
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37

Sadigurschi, Noa, Gilad Scrift, Johannes Hirrlinger, and Hava M. Golan. "Genetic impairment of folate metabolism regulates cortical interneurons and social behavior." Frontiers in Neuroscience 17 (June 28, 2023). http://dx.doi.org/10.3389/fnins.2023.1203262.

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IntroductionThe implications of folate deficiency in neuropsychiatric disorders were demonstrated in numerous studies. Genetic deficiency in a key folate metabolism enzyme, MTHFR, is an example of the interaction between genetic and environmental risk factors: the maternal MTHFR deficiency governs in-utero nutrient availability, and the embryo’s Mthfr genotype influences its ability to metabolize folates. Here, we explore how the maternal and offspring Mthfr genotypes affect cortical interneuron densities and distributions, mouse social outcome, and the relation of the different interneuron pa
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38

Taxidis, Jiannis, Blake Madruga, Karen Safaryan, et al. "Voltage imaging reveals hippocampal inhibitory dynamics shaping pyramidal memory-encoding sequences." Nature Neuroscience, July 22, 2025. https://doi.org/10.1038/s41593-025-02016-y.

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Abstract Hippocampal spiking sequences encode and link behaviorally relevant information across time. How inhibition sculpts these sequences remains unclear. We performed longitudinal voltage imaging of CA1 parvalbumin- and somatostatin-expressing interneurons in mice performing an odor-cued working memory task. Unlike pyramidal odor-specific sequences that encode odor and time throughout a delay period, interneurons encoded odor delivery, but not odor identity or delay time. Odor-triggered inhibition was exerted by stable numbers of interneurons across days, with constant cell turnover, indep
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Bechelli, Lucila, Eugenia Tomasella, Sofia Lopez Cardoso, Martina Belmonte, and Diego M. Gelman. "Selective dopamine D2 receptor deletion from Nkx6.2 expressing cells causes impaired cognitive, motivation and anxiety phenotypes in mice." Scientific Reports 13, no. 1 (2023). http://dx.doi.org/10.1038/s41598-023-46954-8.

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AbstractAbnormal dopamine neurotransmission is a common trait of some psychiatric diseases, like schizophrenia or bipolar disorder. Excessive dopaminergic tone in subcortical brain regions is associated with psychotic episodes, while reduced prefrontal dopaminergic activity is associated with impaired cognitive performance and reduced motivation, among other symptoms. Inhibitory interneurons expressing the calcium binding protein parvalbumin are particularly affected in both schizophrenia and bipolar disorder, as they set a fine-tuned physiological inhibitory/excitatory balance. Parvalbumin an
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40

Reid, Hannah M. O., Owen Trepanier, Allyson Gross, et al. "Prenatal ethanol and cannabis exposure have sex‐ and region‐specific effects on somatostatin and neuropeptide Y interneurons in the rat hippocampus." Alcohol, Clinical and Experimental Research, May 24, 2024. http://dx.doi.org/10.1111/acer.15350.

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AbstractBackgroundCannabis is increasingly being legalized and socially accepted around the world and is often used with alcohol in social settings. We recently showed that in utero exposure to both substances can alter the density of parvalbumin‐expressing interneurons in the hippocampus. Here we investigate the effects of in utero alcohol and cannabis exposure, alone or in combination, on somatostatin‐ and neuropeptide Y‐positive (NPY) interneurons. These are separate classes of interneurons important for network synchrony and inhibition in the hippocampus.MethodsA 2 (Ethanol, Air) × 2 (tetr
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41

Fei, Fan, Xia Wang, Xukun Fan, et al. "Circuit reorganization of subicular cell-type-specific interneurons in temporal lobe epilepsy." Journal of Neuroscience, December 10, 2024, e0760242024. https://doi.org/10.1523/jneurosci.0760-24.2024.

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The subiculum represents a crucial brain pivot in regulating seizure generalization in temporal lobe epilepsy (TLE), primarily through synergy of local GABAergic and long-projecting glutamatergic signaling. However, little is known about how subicular GABAergic interneurons are involved in a cell-type-specific way. Here, employing Ca2+fiber photometry, retrograde monosynaptic viral tracing and chemogenetics in epilepsy models of both male and female mice, we elucidate circuit reorganization patterns mediated by subicular cell-type-specific interneurons and delineate their functional disparitie
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42

Asgarian, Zeinab, Marcio Guiomar Oliveira, Agata Stryjewska, et al. "MTG8 interacts with LHX6 to specify cortical interneuron subtype identity." Nature Communications 13, no. 1 (2022). http://dx.doi.org/10.1038/s41467-022-32898-6.

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AbstractCortical interneurons originating in the embryonic medial ganglionic eminence (MGE) diverge into a range of different subtypes found in the adult mouse cerebral cortex. The mechanisms underlying this divergence and the timing when subtype identity is set up remain unclear. We identify the highly conserved transcriptional co-factor MTG8 as being pivotal in the development of a large subset of MGE cortical interneurons that co-expresses Somatostatin (SST) and Neuropeptide Y (NPY). MTG8 interacts with the pan-MGE transcription factor LHX6 and together the two factors are sufficient to pro
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Cheng, Bokun, Deep R. Sharma, Ajeet Kumar, et al. "SHH activation restores interneurons and cognitive function in newborns with intraventricular haemorrhage." Brain, July 22, 2022. http://dx.doi.org/10.1093/brain/awac271.

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Abstract Premature infants with germinal matrix hemorrhage-intraventricular hemorrhage (GMH-IVH) suffer from neurobehavioral deficits as they enter childhood and adolescence. Yet the underlying mechanisms remain unclear. Impaired development and function of interneurons contribute to neuropsychiatric disorders. Therefore, we hypothesized that the occurrence of IVH would reduce interneuron neurogenesis in the medial ganglionic eminence and diminish the population of parvalbumin+ and somatostatin+ cortical interneurons. Since Sonic Hedgehog promotes the production of cortical interneurons, we al
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Shapiro, Jared T., Nicole M. Michaud, Jillian L. King, and Nathan A. Crowder. "Optogenetic Activation of Interneuron Subtypes Modulates Visual Contrast Responses of Mouse V1 Neurons." Cerebral Cortex, August 19, 2021. http://dx.doi.org/10.1093/cercor/bhab269.

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Abstract Interneurons are critical for information processing in the cortex. In vitro optogenetic studies in mouse primary visual cortex (V1) have sketched the connectivity of a local neural circuit comprising excitatory pyramidal neurons and distinct interneuron subtypes that express parvalbumin (Pvalb+), somatostatin (SOM+), or vasoactive intestinal peptide (VIP+). However, in vivo studies focusing on V1 orientation tuning have ascribed discrepant computational roles to specific interneuron subtypes. Here, we sought to clarify the differences between interneuron subtypes by examining the eff
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Rhodes, Christopher T., Dhanya Asokumar, Mira Sohn, et al. "Loss of Ezh2 in the medial ganglionic eminence alters interneuron fate, cell morphology and gene expression profiles." Frontiers in Cellular Neuroscience 18 (February 14, 2024). http://dx.doi.org/10.3389/fncel.2024.1334244.

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IntroductionEnhancer of zeste homolog 2 (Ezh2) is responsible for trimethylation of histone 3 at lysine 27 (H3K27me3), resulting in repression of gene expression. Here, we explore the role of Ezh2 in forebrain GABAergic interneuron development.MethodsWe removed Ezh2 in the MGE by generating Nkx2-1Cre;Ezh2 conditional knockout mice. We then characterized changes in MGE-derived interneuron fate and electrophysiological properties in juvenile mice, as well as alterations in gene expression, chromatin accessibility and histone modifications in the MGE.ResultsLoss of Ezh2 increases somatostatin-exp
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Girgenti, Matthew J., Eric S. Wohleb, Sameet Mehta, Sriparna Ghosal, Manoela V. Fogaca, and Ronald S. Duman. "Prefrontal cortex interneurons display dynamic sex-specific stress-induced transcriptomes." Translational Psychiatry 9, no. 1 (2019). http://dx.doi.org/10.1038/s41398-019-0642-z.

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Abstract γ-aminobutyric acid (GABA) inhibitory interneurons play a key role in efferent and afferent control of principle neuron activity in the prefrontal cortex (PFC), thereby regulating signal integrity of cognitive and behavioral processes. Recent evidence suggests that specific subtypes of interneurons in the PFC mediate stress-induced depressive-like behaviors. Abnormalities of GABA interneurons, particularly the somatostatin (human, SST; mouse, Sst) subtype, have been reported in postmortem brains of depressed subjects and include sex differences that could explain the increased inciden
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Christodoulou, Ourania, Ioannis Maragkos, Vassiliki Antonakou, and Myrto Denaxa. "The development of MGE-derived cortical interneurons: An Lhx6 tale." International Journal of Developmental Biology, 2022. http://dx.doi.org/10.1387/ijdb.210185md.

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The cerebral cortex contains two main neuronal cell populations, the excitatory pyramidal neurons and the inhibitory interneurons, which constitute 20-30% of all cortical neurons. Cortical interneurons are characterized by a remarkable morphological, molecular and functional diversity. A swathe of research activity in the last 20 years aimed to determine how cortical interneurons acquire their mature cellular and functional features, identified a number of transcription factors that function at different stages of interneuron development. Here, we review all current knowledge concerning the mu
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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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Ochi, Ryo, Fumihiko Ueno, Mutsuki Sakuma, et al. "Patterns of functional connectivity alterations induced by alcohol reflect somatostatin interneuron expression in the human cerebral cortex." Scientific Reports 12, no. 1 (2022). http://dx.doi.org/10.1038/s41598-022-12035-5.

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AbstractAcute alcohol administration affects functional connectivity, yet the underlying mechanism is unknown. Previous work suggested that a moderate dose of alcohol reduces the activity of gamma-aminobutyric acidergic (GABAergic) interneurons, thereby leading to a state of pyramidal disinhibition and hyperexcitability. The present study aims to relate alcohol-induced changes in functional connectivity to regional genetic markers of GABAergic interneurons. Healthy young adults (N = 15, 5 males) underwent resting state functional MRI scanning prior to alcohol administration, immediately and 90
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Miri, Mitra L., Martin Vinck, Rima Pant, and Jessica A. Cardin. "Altered hippocampal interneuron activity precedes ictal onset." eLife 7 (November 2, 2018). http://dx.doi.org/10.7554/elife.40750.

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Although failure of GABAergic inhibition is a commonly hypothesized mechanism underlying seizure disorders, the series of events that precipitate a rapid shift from healthy to ictal activity remain unclear. Furthermore, the diversity of inhibitory interneuron populations poses a challenge for understanding local circuit interactions during seizure initiation. Using a combined optogenetic and electrophysiological approach, we examined the activity of identified mouse hippocampal interneuron classes during chemoconvulsant seizure induction in vivo. Surprisingly, synaptic inhibition from parvalbu
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