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Traumatic alterations in GABA signaling disrupt hippocampal network activity in the developing brain

Severe head trauma causes widespread neuronal shear injuries and acute seizures. Shearing of neural processes might contribute to seizures by disrupting the transmembrane ion gradients that subserve normal synaptic signaling. To test this possibility, we investigated changes in intracellular chlorid... Full description

Journal Title: The Journal of neuroscience : the official journal of the Society for Neuroscience 21 March 2012, Vol.32(12), pp.4017-31
Main Author: Dzhala, Volodymyr
Other Authors: Valeeva, Guzel , Glykys, Joseph , Khazipov, Rustem , Staley, Kevin
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1529-2401 ; PMID: 22442068 Version:1 ; DOI: 10.1523/JNEUROSCI.5139-11.2012
Link: http://pubmed.gov/22442068
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recordid: medline22442068
title: Traumatic alterations in GABA signaling disrupt hippocampal network activity in the developing brain
format: Article
creator:
  • Dzhala, Volodymyr
  • Valeeva, Guzel
  • Glykys, Joseph
  • Khazipov, Rustem
  • Staley, Kevin
subjects:
  • Hippocampus
  • Brain Injuries -- Pathology
  • Nerve Net -- Drug Effects
  • Neurons -- Drug Effects
  • Signal Transduction -- Physiology
  • Gamma-Aminobutyric Acid -- Pharmacology
ispartof: The Journal of neuroscience : the official journal of the Society for Neuroscience, 21 March 2012, Vol.32(12), pp.4017-31
description: Severe head trauma causes widespread neuronal shear injuries and acute seizures. Shearing of neural processes might contribute to seizures by disrupting the transmembrane ion gradients that subserve normal synaptic signaling. To test this possibility, we investigated changes in intracellular chloride concentration ([Cl(-)](i)) associated with the widespread neural shear injury induced during preparation of acute brain slices. In hippocampal slices and intact hippocampal preparations from immature CLM-1 mice, increases in [Cl(-)](i) correlated with disruption of neural processes and biomarkers of cell injury. Traumatized neurons with higher [Cl(-)](i) demonstrated excitatory GABA signaling, remained synaptically active, and facilitated network activity as assayed by the frequency of extracellular action potentials and spontaneous network-driven oscillations. These data support a more inhibitory role for GABA in the unperturbed immature brain, demonstrate the utility of the acute brain slice preparation for the study of the consequences of trauma, and provide potential mechanisms for both GABA-mediated excitatory network events in the slice preparation and early post-traumatic seizures.
language: eng
source:
identifier: E-ISSN: 1529-2401 ; PMID: 22442068 Version:1 ; DOI: 10.1523/JNEUROSCI.5139-11.2012
fulltext: fulltext
issn:
  • 15292401
  • 1529-2401
url: Link


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titleTraumatic alterations in GABA signaling disrupt hippocampal network activity in the developing brain
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subjectHippocampus ; Brain Injuries -- Pathology ; Nerve Net -- Drug Effects ; Neurons -- Drug Effects ; Signal Transduction -- Physiology ; Gamma-Aminobutyric Acid -- Pharmacology
descriptionSevere head trauma causes widespread neuronal shear injuries and acute seizures. Shearing of neural processes might contribute to seizures by disrupting the transmembrane ion gradients that subserve normal synaptic signaling. To test this possibility, we investigated changes in intracellular chloride concentration ([Cl(-)](i)) associated with the widespread neural shear injury induced during preparation of acute brain slices. In hippocampal slices and intact hippocampal preparations from immature CLM-1 mice, increases in [Cl(-)](i) correlated with disruption of neural processes and biomarkers of cell injury. Traumatized neurons with higher [Cl(-)](i) demonstrated excitatory GABA signaling, remained synaptically active, and facilitated network activity as assayed by the frequency of extracellular action potentials and spontaneous network-driven oscillations. These data support a more inhibitory role for GABA in the unperturbed immature brain, demonstrate the utility of the acute brain slice preparation for the study of the consequences of trauma, and provide potential mechanisms for both GABA-mediated excitatory network events in the slice preparation and early post-traumatic seizures.
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abstractSevere head trauma causes widespread neuronal shear injuries and acute seizures. Shearing of neural processes might contribute to seizures by disrupting the transmembrane ion gradients that subserve normal synaptic signaling. To test this possibility, we investigated changes in intracellular chloride concentration ([Cl(-)](i)) associated with the widespread neural shear injury induced during preparation of acute brain slices. In hippocampal slices and intact hippocampal preparations from immature CLM-1 mice, increases in [Cl(-)](i) correlated with disruption of neural processes and biomarkers of cell injury. Traumatized neurons with higher [Cl(-)](i) demonstrated excitatory GABA signaling, remained synaptically active, and facilitated network activity as assayed by the frequency of extracellular action potentials and spontaneous network-driven oscillations. These data support a more inhibitory role for GABA in the unperturbed immature brain, demonstrate the utility of the acute brain slice preparation for the study of the consequences of trauma, and provide potential mechanisms for both GABA-mediated excitatory network events in the slice preparation and early post-traumatic seizures.
doi10.1523/JNEUROSCI.5139-11.2012
pmid22442068
issn02706474
date2012-03-21