Transcriptional dysregulation of γ-aminobutyric acid transporter in parvalbumin-containing inhibitory neurons in the prefrontal cortex in schizophrenia.

Abstract	Parvalbumin (PV)-containing neurons are functionally compromised in schizophrenia. Using double in situ hybridization in postmortem human prefrontal cortex, we found that the messenger RNA (mRNA) for the γ-aminobutyric acid (GABA) transporter GAT-1 was undetectable in 22-41% of PV neurons in layers 3-4 in schizophrenia. In the remaining PV neurons with detectable GAT-1 mRNA, transcript expression was decreased by 26% in layer 3. Hence, the dysfunction of PV neurons involves the molecular dysregulation of presynaptic GABA reuptake.
Authors	Byron K Y Bitanihirwe, Tsung-Ung W Woo
Journal	Psychiatry research (Psychiatry Res) Vol. 220 Issue 3 Pg. 1155-9 (Dec 30 2014) ISSN: 1872-7123 [Electronic] Ireland
PMID	25312391 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)
Copyright	Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
Chemical References	GABA Plasma Membrane Transport Proteins Parvalbumins RNA, Messenger gamma-Aminobutyric Acid
Topics	Adult Aged Aged, 80 and over Female GABA Plasma Membrane Transport Proteins (genetics) Gene Expression Regulation Humans Male Middle Aged Neural Inhibition (genetics, physiology) Neurons (metabolism) Parvalbumins (metabolism) Prefrontal Cortex (pathology, physiopathology) RNA, Messenger (metabolism) Schizophrenia (genetics, pathology, physiopathology) Synaptic Transmission (physiology) gamma-Aminobutyric Acid (metabolism)

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