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Tytuł pozycji:

Subregion-Specific Impacts of Genetic Loss of Diazepam Binding Inhibitor on Synaptic Inhibition in the Murine Hippocampus.

Tytuł :
Subregion-Specific Impacts of Genetic Loss of Diazepam Binding Inhibitor on Synaptic Inhibition in the Murine Hippocampus.
Autorzy :
Courtney CD; Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, United States.
Christian CA; Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, United States; Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL, United States; Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign, Urbana, IL, United States. Electronic address: .
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Źródło :
Neuroscience [Neuroscience] 2018 Sep 15; Vol. 388, pp. 128-138. Date of Electronic Publication: 2018 Jul 19.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Publication: [New York?] : Elsevier Science
Original Publication: Oxford, Elmsford, N. Y., Pergamon Press
MeSH Terms :
Diazepam Binding Inhibitor/*deficiency
Hippocampus/*metabolism
Inhibitory Postsynaptic Potentials/*physiology
Neurons/*metabolism
Animals ; Central Nervous System Agents/pharmacology ; Diazepam/pharmacology ; Diazepam Binding Inhibitor/antagonists & inhibitors ; Diazepam Binding Inhibitor/genetics ; Female ; Flumazenil/pharmacology ; Hippocampus/drug effects ; Inhibitory Postsynaptic Potentials/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Miniature Postsynaptic Potentials/drug effects ; Miniature Postsynaptic Potentials/physiology ; Neurons/drug effects ; Receptors, GABA-A/metabolism ; Tissue Culture Techniques
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Grant Information :
R01 NS105825 United States NS NINDS NIH HHS
Contributed Indexing :
Keywords: GABA*; benzodiazepine*; diazepam*; electrophysiology*; flumazenil*; paired-pulse ratio*
Substance Nomenclature :
0 (Central Nervous System Agents)
0 (Diazepam Binding Inhibitor)
0 (Receptors, GABA-A)
40P7XK9392 (Flumazenil)
Q3JTX2Q7TU (Diazepam)
Entry Date(s) :
Date Created: 20180722 Date Completed: 20190329 Latest Revision: 20190329
Update Code :
20210210
PubMed Central ID :
PMC6281174
DOI :
10.1016/j.neuroscience.2018.07.012
PMID :
30031126
Czasopismo naukowe
Benzodiazepines are commonly prescribed to treat neurological conditions including epilepsy, insomnia, and anxiety. The discovery of benzodiazepine-specific binding sites on γ-aminobutyric acid type-A receptors (GABA A Rs) led to the hypothesis that the brain may produce endogenous benzodiazepine-binding site ligands. An endogenous peptide, diazepam binding inhibitor (DBI), which can bind these sites, is thought to be capable of both enhancing and attenuating GABAergic transmission in different brain regions. However, the role that DBI plays in modulating GABA A Rs in the hippocampus remains unclear. Here, we investigated the role of DBI in modulating synaptic inhibition in the hippocampus using a constitutive DBI knockout mouse. Miniature and evoked inhibitory postsynaptic currents (mIPSCs, eIPSCs) were recorded from CA1 pyramidal cells and dentate gyrus (DG) granule cells. Loss of DBI signaling increased mIPSC frequency and amplitude in CA1 pyramidal cells from DBI knockout mice compared to wild-types. In DG granule cells, conversely, the loss of DBI decreased mIPSC amplitude and increased mIPSC decay time, indicating bidirectional modulation of GABA A R-mediated transmission in specific subregions of the hippocampus. eIPSC paired-pulse ratios were consistent across genotypes, suggesting that alterations in mIPSC frequency were not due to changes in presynaptic release probability. Furthermore, cells from DBI knockout mice did not display altered responsiveness to pharmacological applications of diazepam, a benzodiazepine, nor flumazenil, a benzodiazepine-binding site antagonist. These results provide evidence that genetic loss of DBI alters synaptic inhibition in the adult hippocampus, and that the direction of DBI-mediated modulation can vary discretely between specific subregions of the same brain structure.
(Copyright © 2018 IBRO. Published by Elsevier Ltd. All rights reserved.)

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