Morphine coordinates SST and PV interneurons in the prelimbic cortex to disinhibit pyramidal neurons and enhance reward DOI Creative Commons
Changyou Jiang,

Xueying Wang,

Qiumin Le

et al.

Molecular Psychiatry, Journal Year: 2019, Volume and Issue: 26(4), P. 1178 - 1193

Published: Aug. 14, 2019

Abstract Opioids, such as morphine, are clinic analgesics which induce euphoria. Morphine exposure modifies the excitability and functional interactions between neurons, while underlying cellular molecular mechanisms, especially how morphine assembles heterogeneous interneurons (INs) in prelimbic cortex (PrL) to mediate disinhibition reward, not clear. Using approaches of optogenetics, electrophysiology, cell type-specific RNA-seq, we show that attenuates inhibitory synaptic transmission from parvalbumin + (PV)-INs onto pyramidal neurons PrL via μ-opioid receptor (MOR) PV-INs. Meanwhile, enhances inputs somatostatin (SST)-INs PV-INs, thus disinhibits δ-opioid (DOR)-dependent Rac1 upregulation SST-INs. We MOR PV-INs is required for morphine-induced behavioral sensitization, DOR well activity SST-INs conditioned place preference hyper-locomotion. These results reveal SST- functioning a disinhibitory architecture, coordinated by different opioid receptors disinhibit enhance reward.

Language: Английский

Medial prefrontal cortex in neurological diseases DOI Open Access
Pan Xu, Ai Chen, Yipeng Li

et al.

Physiological Genomics, Journal Year: 2019, Volume and Issue: 51(9), P. 432 - 442

Published: Aug. 2, 2019

The medial prefrontal cortex (mPFC) is a crucial cortical region that integrates information from numerous and subcortical areas converges updated to output structures. It plays essential roles in the cognitive process, regulation of emotion, motivation, sociability. Dysfunction mPFC has been found various neurological psychiatric disorders, such as depression, anxiety schizophrenia, autism spectrum Alzheimer's disease, Parkinson's addiction. In present review, we summarize preclinical clinical studies illustrate role these diseases.

Language: Английский

Citations

255

Anterior cingulate cortex dysfunction underlies social deficits in Shank3 mutant mice DOI
Baolin Guo, Jing Chen, Qian Chen

et al.

Nature Neuroscience, Journal Year: 2019, Volume and Issue: 22(8), P. 1223 - 1234

Published: July 22, 2019

Language: Английский

Citations

225

Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications DOI
Zhen Yan, Benjamin Rein

Molecular Psychiatry, Journal Year: 2021, Volume and Issue: 27(1), P. 445 - 465

Published: April 19, 2021

Language: Английский

Citations

196

Prefrontal somatostatin interneurons encode fear memory DOI
Kirstie A. Cummings, Roger L. Clem

Nature Neuroscience, Journal Year: 2019, Volume and Issue: 23(1), P. 61 - 74

Published: Dec. 16, 2019

Language: Английский

Citations

190

Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression-like states DOI
Xia Zhu,

Hao-Di Tang,

Wanying Dong

et al.

Nature Neuroscience, Journal Year: 2021, Volume and Issue: 24(4), P. 542 - 553

Published: March 8, 2021

Language: Английский

Citations

108

Neocortical somatostatin neuron diversity in cognition and learning DOI Creative Commons
Eunsol Park, Matthew B. Mosso, Alison L. Barth

et al.

Trends in Neurosciences, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

2

Prefrontal parvalbumin interneurons require juvenile social experience to establish adult social behavior DOI Creative Commons
Lucy Bicks, Kazuhiko Yamamuro, Meghan E. Flanigan

et al.

Nature Communications, Journal Year: 2020, Volume and Issue: 11(1)

Published: Feb. 21, 2020

Abstract Social isolation during the juvenile critical window is detrimental to proper functioning of prefrontal cortex (PFC) and establishment appropriate adult social behaviors. However, specific circuits that undergo experience-dependent maturation regulate behavior are poorly understood. We identify a activation pattern parvalbumin-positive interneurons (PVIs) in dorsal-medial PFC (dmPFC) prior an active bout, or bout initiated by focal mouse, but not passive when mice explored stimulus mouse. Optogenetic chemogenetic manipulation reveals brief dmPFC-PVI triggers approach promote sociability. Juvenile decouples from subsequent freezing functional process dmPFC-PVIs juvenile-to-adult transition. Chemogenetic activity animal mitigates isolation-induced deficits. Therefore, linked long-term impacts on behavior.

Language: Английский

Citations

133

Strong inhibitory signaling underlies stable temporal dynamics and working memory in spiking neural networks DOI

Robert Kim,

Terrence J. Sejnowski

Nature Neuroscience, Journal Year: 2020, Volume and Issue: 24(1), P. 129 - 139

Published: Dec. 7, 2020

Language: Английский

Citations

126

eIF2α controls memory consolidation via excitatory and somatostatin neurons DOI
Vijendra Sharma,

Rapita Sood,

Abdessattar Khlaifia

et al.

Nature, Journal Year: 2020, Volume and Issue: 586(7829), P. 412 - 416

Published: Oct. 7, 2020

Language: Английский

Citations

106

Neural circuits and activity dynamics underlying sex-specific effects of chronic social isolation stress DOI Creative Commons
Tao Tan, Wei Wang,

Tiaotiao Liu

et al.

Cell Reports, Journal Year: 2021, Volume and Issue: 34(12), P. 108874 - 108874

Published: March 1, 2021

Exposure to prolonged stress in critical developmental periods induces heightened vulnerability psychiatric disorders, which may have sex-specific consequences. Here we investigate the neuronal circuits mediating behavioral changes mice after chronic adolescent social isolation stress. Escalated aggression is exhibited stressed males, while withdrawal shown females. In vivo multichannel recordings of free-moving animals indicate that pyramidal neurons prefrontal cortex (PFC) from males exhibit significantly decreased spike activity during aggressive attacks, PFC females show a blunted increase discharge rates sociability tests. Chemogenetic and electrophysiological evidence shows hypofunctioning BLA principal neuron hyperactivity contribute elevated VTA dopamine hypoactivity diminished These results establish framework for understanding circuit physiological mechanisms underlying divergent effects

Language: Английский

Citations

87