Adenosine-mediated synaptic depression and EPSP/spike dissociation following high potassium-induced depolarization in rat hippocampal slices

Youn-Kwan Park, Eun Sheb Shim, Jae In Oh, Joo-Han Kim, Yong Gu Chung

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Simultaneous recordings of orthodromic PS, fEPSP and antidromic PS revealed EPSP/spike (E-S) dissociation, indicating a conversion of input/output relations from early and brief excitability to a late and prolonged depression during the recovery from depolarization induced by high levels of potassium. E-S potentiation was partially attenuated by pre-treating the slices with BAPTA-AM and lidocaine and totally eliminated by a submaximal concentration of muscimol. The time lag for recovery was decreased by the GABAA antagonist and completely eliminated by the A1 antagonist. From these observations, we conclude that Ca2+ dependent inhibitory suppression is the main cause of a brief period of E-S potentiation, and accumulation of adenosine is the mechanism responsible for prolonged depression of synaptic transmission.

Original languageEnglish
Pages (from-to)237-243
Number of pages7
JournalBrain Research
Volume975
Issue number1-2
DOIs
Publication statusPublished - 2003 Jun 13

Fingerprint

Excitatory Postsynaptic Potentials
Adenosine
Potassium
GABA-A Receptor Antagonists
Muscimol
Lidocaine
Synaptic Transmission

Keywords

  • Depolarization
  • EPSP/spike dissociation
  • High K irrigation
  • Hippocampus

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

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abstract = "Simultaneous recordings of orthodromic PS, fEPSP and antidromic PS revealed EPSP/spike (E-S) dissociation, indicating a conversion of input/output relations from early and brief excitability to a late and prolonged depression during the recovery from depolarization induced by high levels of potassium. E-S potentiation was partially attenuated by pre-treating the slices with BAPTA-AM and lidocaine and totally eliminated by a submaximal concentration of muscimol. The time lag for recovery was decreased by the GABAA antagonist and completely eliminated by the A1 antagonist. From these observations, we conclude that Ca2+ dependent inhibitory suppression is the main cause of a brief period of E-S potentiation, and accumulation of adenosine is the mechanism responsible for prolonged depression of synaptic transmission.",
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AU - Park, Youn-Kwan

AU - Shim, Eun Sheb

AU - Oh, Jae In

AU - Kim, Joo-Han

AU - Chung, Yong Gu

PY - 2003/6/13

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