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Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
10:13

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

Published on: July 31, 2017

Diazepam neuroprotection in excitotoxic and oxidative stress involves a mitochondrial mechanism additional to the

Anna Sarnowska1, Małgorzata Beresewicz, Barbara Zabłocka

  • 1NeuroRepair Department, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland. a_sarnowska@tlen.pl

Neurochemistry International
|May 12, 2009
PubMed

Insights

Diazepam protects hippocampal neurons from death by reducing mitochondrial cytochrome c release, not just by lowering body temperature. This neuroprotection involves GABA(A) and TSPO receptors.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Neuronal death in the CA1 hippocampus sector is a critical factor in ischemic brain injury.
  • Diazepam is known to have neuroprotective effects, but its precise mechanisms are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying diazepam's neuroprotection in CA1 hippocampal neurons.
  • To differentiate the neuroprotective effects of diazepam from drug-induced hypothermia.

Main Methods:

  • In vivo transient global ischemia model in gerbils and in vitro models using rat hippocampal slices subjected to NMDA or oxidative stress.
  • Monitoring body temperature changes and neuronal survival rates post-ischemia.
  • Assessing the effect of diazepam on cytochrome c efflux from mitochondria.

Main Results:

  • Diazepam significantly increased CA1 neuronal survival in vivo and in vitro, independent of hypothermia.
  • Neuroprotection occurred within a specific dose range (0.5-10 microM) and was observed even with GABA(A) receptor blockade.
  • Diazepam reduced cytochrome c efflux from mitochondria in stressed neurons and isolated mitochondria.

Conclusions:

  • Diazepam's neuroprotective effects extend beyond hypothermia, involving mechanisms beyond GABA(A) receptor agonism.
  • The translocator protein (TSPO) may play a role in diazepam-mediated neuroprotection.
  • Diazepam's action on mitochondrial pathways is a key component of its neuroprotective strategy.

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