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Loss of dysbindin-1 affects GABAergic transmission in the PFC.

Authors
  • Trantham-Davidson, H1
  • Lavin, A2
  • 1 Department of Neuroscience, MUSC, Charleston, SC, 29425, USA.
  • 2 Department of Neuroscience, MUSC, Charleston, SC, 29425, USA. [email protected]
Type
Published Article
Journal
Psychopharmacology
Publication Date
Nov 01, 2019
Volume
236
Issue
11
Pages
3291–3300
Identifiers
DOI: 10.1007/s00213-019-05285-1
PMID: 31201475
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

It has been shown that dystrobrevin-binding protein 1 gene that encodes the protein dysbindin-1 is associated with risk for cognitive deficits, and studies have shown decreases in glutamate and correlated decreases in dysbindin-1 protein in the prefrontal cortex (PFC) and hippocampus of post-mortem tissue from schizophrenia patients. The PFC and the hippocampus have been shown to play a fundamental role in cognition, and studies in dysbindin-1 null mice have shown alterations in NMDAR located in pyramidal neurons as well as perturbation in LTP and cognitive deficits. The balance between excitatory and inhibitory transmission is crucial for normal cognitive functions; however, there is a dearth of information regarding the effects of loss of dysbindin-1 in GABAergic transmission. Using in vitro whole-cell clamp recordings, Western blots, and immunohistochemistry, we report here that dysbindin-1-deficient mice exhibit a significant decrease in the frequency of sIPSCs and in the amplitude of mIPSCs and significant decreases in PV staining and protein level. These results suggest that loss of dysbindin-1 affects GABAergic transmission at pre- and postsynaptic level and decreases parvalbumin markers.

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