Faculty Opinions recommendation of Neurotensin activates GABAergic interneurons in the prefrontal cortex.

2005 ◽  
Author(s):  
Michael Owens
Keyword(s):  
Prefrontal Cortex ◽  
Gabaergic Interneurons

A whole-brain map of long-range inputs to GABAergic interneurons in the mouse medial prefrontal cortex

2019 ◽  
Vol 22 (8) ◽  
pp. 1357-1370 ◽  
Author(s):  
Qingtao Sun ◽  
Xiangning Li ◽  
Miao Ren ◽  
Mengting Zhao ◽  
Qiuyuan Zhong ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Long Range ◽  
Medial Prefrontal Cortex ◽  
Gabaergic Interneurons ◽  
Whole Brain

scholarly journals Characterization of GABAergic Marker Expression in the Chronic Unpredictable Stress Model of Depression

2017 ◽  
Vol 1 ◽  
pp. 247054701772045 ◽  
Author(s):  
Mounira Banasr ◽  
Ashley Lepack ◽  
Corey Fee ◽  
Vanja Duric ◽  
Jaime Maldonado-Aviles ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Protein Expression ◽  
Neuropeptide Y ◽  
Chronic Stress ◽  
Gabaergic Interneurons ◽  
Chronic Unpredictable Stress ◽  
Major Depressive

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 unpredictable stress exposure on the expression of GABA-synthesizing enzymes (GAD65 and GAD67), calcium-binding proteins (calbindin, parvalbumin, and calretinin), and neuropeptides co-expressed in GABAergic neurons (somatostatin, neuropeptide Y, vasoactive intestinal peptide, and cholecystokinin) in the prefrontal cortex and hippocampus of rats. We also investigated the effects of corticosterone and dexamethasone exposure on these markers in vitro in primary cortical and hippocampal cultures. Results We found that chronic unpredictable stress induced significant reductions of GAD67 protein levels in both the prefrontal cortex and hippocampus of chronic unpredictable stress-exposed rats but did not detect changes in GAD65 protein expression. Similar protein expression changes were found in vitro in cortical neurons. In addition, our results provide clear evidence of reduced markers of interneuron population(s), namely somatostatin and neuropeptide Y, in the prefrontal cortex, suggesting these cell types may be selectively vulnerable to chronic stress. Conclusion Together, this work highlights that chronic stress induces regional and cell type-selective effects on GABAergic interneurons in rats. These findings provide additional supporting evidence that stress-induced GABA neuron dysfunction and cell vulnerability play critical roles in the pathophysiology of stress-related illnesses, including major depressive disorder.

scholarly journals Polysialylated NCAM and EphrinA/EphA Regulate Synaptic Development of GABAergic Interneurons in Prefrontal Cortex

2012 ◽  
Vol 23 (1) ◽  
pp. 162-177 ◽  
Author(s):  
Leann H. Brennaman ◽  
Xuying Zhang ◽  
Hanjun Guan ◽  
Jason W. Triplett ◽  
Arthur Brown ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Gabaergic Interneurons ◽  
Synaptic Development

Mechanisms of Dopamine Activation of Fast-Spiking Interneurons That Exert Inhibition in Rat Prefrontal Cortex

2002 ◽  
Vol 88 (6) ◽  
pp. 3150-3166 ◽  
Author(s):  
Natalia Gorelova ◽  
Jeremy K. Seamans ◽  
Charles R. Yang
Keyword(s):  
Prefrontal Cortex ◽  
Receptor Antagonist ◽  
Pyramidal Neurons ◽  
Sch 23390 ◽  
Membrane Depolarization ◽  
Inward Rectifier ◽  
Repetitive Firing ◽  
Gabaergic Interneurons ◽  
Fast Spiking

Prefrontal cortical dopamine (DA) modulates pyramidal cell excitability directly and indirectly by way of its actions on local circuit GABAergic interneurons. DA modulation of interneuronal functions is implicated in the computational properties of prefrontal networks during cognitive processes and in schizophrenia. Morphologically and electrophysiologically distinct classes of putative GABAergic interneurons are found in layers II-V of rat prefrontal cortex. Our whole cell patch-clamp study shows that DA induced a direct, TTX-insensitive, reversible membrane depolarization, and increased the excitability of fast-spiking (FS) interneurons. The DA-induced membrane depolarization was reduced significantly by D1/D5 receptor antagonist SCH 23390, but not by the D2 receptor antagonist (−)sulpiride, D4 receptor antagonists U101958 or L-745870, α1-adrenoreceptor antagonist prazosin, or serotoninergic receptor antagonist mianserin. The D1/5 agonists SKF81297 or dihydrexidine, but not D2 agonist quinpirole, also induced a prolonged membrane depolarization. Voltage-clamp analyses of the voltage-dependence of DA-sensitive currents, and the effects of changing [K+]O on reversal potentials of DA responses, revealed that DA suppressed a Cs+-sensitive inward rectifier K+ current and a resting leak K+ current. D1/D5, but not D2 agonists mimicked the suppressive effects of DA on the leak current, but the DA effects on the inward rectifier K+ current were not mimicked by either agonist. In a subgroup of FS interneurons, the slowly inactivating membrane outward rectification evoked by depolarizing voltage steps was also attenuated by DA. Collectively, these data showed that DA depolarizes FS interneurons by suppressing a voltage-independent ‘leak’ K+ current (via D1/D5 receptor mechanism) and an inwardly rectifying K+ current (via unknown DA mechanisms). Additional suppression of a slowly inactivating K+ current led to increase in repetitive firing in response to depolarizing inputs. This D1-induced increase in interneuron excitability enhances GABAergic transmission to PFC pyramidal neurons and could represent a mechanism via which DA suppresses persistent firing of pyramidal neurons in vivo.

Dopamine D5 receptor immunoreactivity is differentially distributed in GABAergic interneurons and pyramidal cells in the rat medial prefrontal cortex

2010 ◽  
Vol 1329 ◽  
pp. 89-102 ◽  
Author(s):  
Satoko Oda ◽  
Hiromasa Funato ◽  
Satomi Adachi-Akahane ◽  
Masanori Ito ◽  
Akiko Okada ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Pyramidal Cells ◽  
Gabaergic Interneurons ◽  
Dopamine D5 Receptor

scholarly journals Chemogenetic Inhibition of Infralimbic Prefrontal Cortex GABA-ergic Parvalbumin Interneurons Attenuates Chronic Stress Adaptions in Male Mice

2019 ◽  
Author(s):  
Nawshaba Nawreen ◽  
Rachel Morano ◽  
Parinaz Mahbod ◽  
Evelin M. Cotella ◽  
Khushali Dalal ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Chronic Stress ◽  
Stress Responses ◽  
Acute Stress ◽  
Forced Swim Test ◽  
Designer Drugs ◽  
Gabaergic Interneurons ◽  
Coping Behaviors ◽  
Passive Coping ◽  
Parvalbumin Interneurons

ABSTRACTHypofunction of the prefrontal cortex (PFC) contributes to stress-related neuropsychiatric illnesses. Mechanisms leading to prefrontal hypoactivity remain to be determined. Prior evidence suggests that enhanced activity of parvalbumin (PV) expressing GABAergic interneurons (INs) play a role in chronic stress related pathologies. In this study, the role of PFC PV INs in stress related phenotypes were explored using Cre inducible inhibitory DREADDs (Designer Receptors Exclusively Activated by Designer Drugs). Mice were first tested in the tail suspension test (TST) to determine the effects of PV IN inhibition during acute stress. Following this, the long term impact of PV IN inhibition during chronic variable stress (CVS) was tested in the forced swim test (FST). Acute PV IN inhibition reduced active (struggling) and increased passive coping behaviors (immobility) in the TST. In contrast, inhibition of PV INs during CVS increased active and reduced passive coping behaviors in the FST. Moreover, chronic inhibition of PV INs attenuated CVS-induced changes in Fos expression in the prelimbic cortex, basolateral amygdala and ventrolateral periaqueductal gray and also prevented adrenal hypertrophy and body weight loss associated with chronic stress. Our results suggest differential roles of PV INs to acute vs chronic stress, indicative of distinct biological mechanisms underlying acute vs. chronic stress responses. Our results also indicate a role for PV INs in driving chronic stress adaptation and support literature evidence suggesting cortical GABAergic interneurons as a therapeutic target in stress related diseases.SIGNIFICANCEStress related diseases are associated with prefrontal hypoactivity, the mechanism of which is currently not known. In this study we showed that by inhibiting prefrontal GABA-ergic Parvalbumin interneurons (PV INs) using DREADDs, we can attenuate some of chronic stress related phenotypes. Additionally, we showed that modulation of PV IN activity during acute vs chronic stress had opposing effects on stress coping strategies, suggesting different underlying mechanisms behind acute vs chronic stress paradigms. Our findings indicate that GABA-ergic PV INs may be involved in driving stress related phenotypes and thereby an important target for treatment of stress-related illnesses. Our data suggest that reducing PV IN activity to promote prefrontal output may be an effective treatment strategy for stress related disorders.

scholarly journals The thalamus regulates retinoic acid signaling and development of parvalbumin interneurons in postnatal mouse prefrontal cortex

2018 ◽  
Author(s):  
Rachel Larsen ◽  
Alatheia Proue ◽  
Earl Parker Scott ◽  
Matthew Christiansen ◽  
Yasushi Nakagawa
Keyword(s):  
Prefrontal Cortex ◽  
Retinoic Acid ◽  
Abnormal Development ◽  
Gabaergic Interneurons ◽  
Retinoic Acid Signaling ◽  
Neuron Development ◽  
Thalamic Input ◽  
Parvalbumin Interneurons ◽  
Genetic Deletion ◽  
Medial Pfc

AbstractAbnormal development of GABAergic interneurons in the prefrontal cortex (PFC) is implicated in a number of psychiatric disorders. Yet, developmental mechanisms for these neurons are poorly understood. Here we show that the retinoic acid-degrading enzyme CYP26B1 is temporally expressed specifically in postnatal frontal cortex in mice, and its genetic deletion results in an increased density of parvalbumin (PV)-expressing interneurons in medial PFC during postnatal development. Furthermore, initiation of Cyp26b1 expression in neonatal PFC depends on the connections between the thalamus and the neocortex. Thus, the thalamus has a postnatal role in regulating PV neuron development in PFC by inducing Cyp26b1 and thereby restricting retinoic acid signaling. Prenatally, the lack of thalamic input causes an aberrant radial distribution of medial ganglionic eminence-derived interneurons throughout the cortex. Therefore, the thalamus controls PV neuron development in PFC both by region-specific and cortex-wide mechanisms.

Prenatal phencyclidine treatment induces behavioral deficits through impairment of GABAergic interneurons in the prefrontal cortex

2016 ◽  
Vol 233 (12) ◽  
pp. 2373-2381 ◽  
Author(s):  
Kazuya Toriumi ◽  
Mika Oki ◽  
Eriko Muto ◽  
Junko Tanaka ◽  
Akihiro Mouri ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Gabaergic Interneurons ◽  
Behavioral Deficits
Sign in / Sign up

Export Citation Format

Share Document