Publication

Dysbindin Deficiency Modifies the Expression of GABA Neuron and Ion Permeation Transcripts in the Developing Hippocampus

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Last modified
  • 02/20/2025
Type of Material
Authors
    Jennifer Larimore, Agnes Scott CollegeStephanie A. Zlatic, Emory UniversityMiranda Arnold, Agnes Scott CollegeKaela S. Singleton, Agnes Scott CollegeRebecca Cross, Agnes Scott CollegeHannah Rudolph, Agnes Scott CollegeMartha V. Bruegge, Agnes Scott CollegeAndrea Sweetman, Agnes Scott CollegeCecilia Garza, Agnes Scott CollegeEli Whisnant, Agnes Scott CollegeVictor Faundez, Emory University
Language
  • English
Date
  • 2017-03-10
Publisher
  • Frontiers Media
Publication Version
Copyright Statement
  • © 2017 Larimore, Zlatic, Arnold, Singleton, Cross, Rudolph, Bruegge, Sweetman, Garza, Whisnant and Faundez.
License
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 1664-8021
Volume
  • 8
Grant/Funding Information
  • This work was supported by grants from the National Institutes of Health NS088503 and the Emory School of Medicine Catalyst Grant to VF.
Supplemental Material (URL)
Abstract
  • The neurodevelopmental factor dysbindin is required for synapse function and GABA interneuron development. Dysbindin protein levels are reduced in the hippocampus of schizophrenia patients. Mouse dysbindin genetic defects and other mouse models of neurodevelopmental disorders share defective GABAergic neurotransmission and, in several instances, a loss of parvalbumin-positive interneuron phenotypes. This suggests that mechanisms downstream of dysbindin deficiency, such as those affecting GABA interneurons, could inform pathways contributing to or ameliorating diverse neurodevelopmental disorders. Here we define the transcriptome of developing wild type and dysbindin null Bloc1s8sdy/sdy mouse hippocampus in order to identify mechanisms downstream dysbindin defects. The dysbindin mutant transcriptome revealed previously reported GABA parvalbumin interneuron defects. However, the Bloc1s8sdy/sdy transcriptome additionally uncovered changes in the expression of molecules controlling cellular excitability such as the cation-chloride cotransporters NKCC1, KCC2, and NCKX2 as well as the potassium channel subunits Kcne2 and Kcnj13. Our results suggest that dysbindin deficiency phenotypes, such as GABAergic defects, are modulated by the expression of molecules controlling the magnitude and cadence of neuronal excitability.
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Keywords
Research Categories
  • Biology, General
  • Biology, Cell

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