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.
Keywords:
Parvalbumin; Schizophrenia; γ-aminobutyric acid transporter-1.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
Publication types
-
Research Support, N.I.H., Extramural
MeSH terms
-
Adult
-
Aged
-
Aged, 80 and over
-
Female
-
GABA Plasma Membrane Transport Proteins / genetics*
-
Gene Expression Regulation*
-
Humans
-
Male
-
Middle Aged
-
Neural Inhibition / genetics*
-
Neural Inhibition / physiology*
-
Neurons / metabolism
-
Parvalbumins / metabolism*
-
Prefrontal Cortex / pathology
-
Prefrontal Cortex / physiopathology*
-
RNA, Messenger / metabolism
-
Schizophrenia / genetics*
-
Schizophrenia / pathology
-
Schizophrenia / physiopathology
-
Synaptic Transmission / physiology
-
gamma-Aminobutyric Acid / metabolism*
Substances
-
GABA Plasma Membrane Transport Proteins
-
Parvalbumins
-
RNA, Messenger
-
gamma-Aminobutyric Acid