Transient recovery of synaptic transmission is related to rapid energy depletion during hypoxia

Research output: Contribution to journalArticle

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Abstract

Transient recovery (TR) of evoked synaptic potential during the late stage of hypoxic hypoglycemia (HH) insult was investigated in rat hippocampal slices using extracellular recording methods. TR was observed in association with a rapid deterioration of antidromic population spikes (aPSs) following HH insult. TR was not elicited in normoglycemic hypoxia (NH), in which a gradual and delayed deterioration of aPSs was noted. TR was not modulated by either Ca2+- or PKC-dependent processes. When a glycolytic inhibitor was added, NH resulted in a rapid deterioration of aPSs and prompted appearance of TR. TR was also seen in slices using lactate to generate energy via oxidative phosphorylation, when hypoxic conditions were subsequently created. Other pharmacological interventions that aimed to cause rapid deterioration of aPSs without depleting energy stores failed to reproduce TR. The evidence thus suggests that the underlying mechanisms of TR appearance during HH insult are highly correlated with rapid energy depletion.

Original languageEnglish
Pages (from-to)1-6
Number of pages6
JournalNeuroscience Letters
Volume400
Issue number1-2
DOIs
Publication statusPublished - 2006 May 29

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Synaptic Transmission
Hypoglycemia
Population
Synaptic Potentials
Oxidative Phosphorylation
Evoked Potentials
Lactic Acid
Pharmacology
Hypoxia

Keywords

  • Hippocampus
  • Hypoglycemia
  • Hypoxia
  • In vitro
  • Synaptic transmission

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Transient recovery of synaptic transmission is related to rapid energy depletion during hypoxia. / Kim, Joo-Han; Park, Youn-Kwan; Kim, Jong Hyun; Kwon, Taek-Hyun; Chung, Hung Seob.

In: Neuroscience Letters, Vol. 400, No. 1-2, 29.05.2006, p. 1-6.

Research output: Contribution to journalArticle

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N2 - Transient recovery (TR) of evoked synaptic potential during the late stage of hypoxic hypoglycemia (HH) insult was investigated in rat hippocampal slices using extracellular recording methods. TR was observed in association with a rapid deterioration of antidromic population spikes (aPSs) following HH insult. TR was not elicited in normoglycemic hypoxia (NH), in which a gradual and delayed deterioration of aPSs was noted. TR was not modulated by either Ca2+- or PKC-dependent processes. When a glycolytic inhibitor was added, NH resulted in a rapid deterioration of aPSs and prompted appearance of TR. TR was also seen in slices using lactate to generate energy via oxidative phosphorylation, when hypoxic conditions were subsequently created. Other pharmacological interventions that aimed to cause rapid deterioration of aPSs without depleting energy stores failed to reproduce TR. The evidence thus suggests that the underlying mechanisms of TR appearance during HH insult are highly correlated with rapid energy depletion.

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