Inhibition of apamin-sensitive calcium dependent potassium channels facilitate the induction of long-term potentiation in the CA1 region of rat hippocampus in vitro

Neurosci Lett. 1998 Sep 4;253(2):91-4. doi: 10.1016/s0304-3940(98)00612-0.

Abstract

Using field potential recording in the CA1-region of rat hippocampal slices we investigated the effect of apamin; a specific antagonist of small conductive calcium activated potassium channels on long-term potentiation (LTP). The experiments revealed that LTP of excitatory postsynaptic potentials induced by a single 100 Hz tetanization was intensified by extracellular application of apamin in a concentration range of 1-200 nM. No effects of apamin on LTP induced by triple 100 Hz tetanization were seen. We conclude that the positive modulation of LTP by apamin is effective in a nanomolar concentration range and dependent upon the employed tetanization. Because it has been shown that apamin-binding sites are affected by learning disorders including Alzheimer's disease, our finding suggests that changes in the sensitivity to apamin may result in memory disorders.

MeSH terms

  • Animals
  • Apamin / pharmacology*
  • Calcium / metabolism*
  • Culture Techniques
  • Dose-Response Relationship, Drug
  • Electric Stimulation
  • Electrodes
  • Excitatory Postsynaptic Potentials / drug effects
  • Hippocampus / cytology
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Long-Term Potentiation / drug effects*
  • Male
  • Potassium Channel Blockers*
  • Potassium Channels / metabolism
  • Rats
  • Rats, Wistar
  • Tetany
  • Time Factors

Substances

  • Potassium Channel Blockers
  • Potassium Channels
  • Apamin
  • Calcium