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Dimemorfan enhances acetylcholine release from rat hippocampal slices

Hui-Hung Wang1, Yueh-Ching Chou, Jyh-Fei Liao

  • 1Department and Institute of Pharmacology, National Yang-Ming University, No. 155, Sec. 2, Li-Nong Street, Taipei, Taiwan.

Brain Research
|April 15, 2004
PubMed

Insights

Dimemorfan, an antitussive drug, enhances acetylcholine release in rat brain regions by acting as a sigma1 receptor agonist. This effect, similar to (+)-SKF-10047, was blocked by the sigma1 receptor antagonist haloperidol.

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Previous research indicated dimemorfan, an antitussive, mitigates amnesia and functions as a sigma1 receptor agonist.
  • Sigma1 receptors are implicated in modulating neurotransmitter release.

Purpose of the Study:

  • To investigate the effect of dimemorfan on acetylcholine release in rat brain slices.
  • To confirm the role of sigma1 receptors in dimemorfan's action on neurotransmitter release.

Main Methods:

  • Rat hippocampal and striatal slices were used to measure KCl-evoked [3H]acetylcholine release.
  • The effects of dimemorfan and (+)-SKF-10047 were assessed in the presence and absence of haloperidol.

Main Results:

  • Dimemorfan (30 microM) and (+)-SKF-10047 (10 microM) significantly increased acetylcholine release in hippocampal slices.
  • This enhancement of acetylcholine release was specifically observed in hippocampal, not striatal, slices.
  • Haloperidol (0.3 microM), a sigma1 receptor antagonist, blocked the effects of both dimemorfan and (+)-SKF-10047.

Conclusions:

  • Dimemorfan enhances acetylcholine release in the rat hippocampus via sigma1 receptor agonism.
  • These findings support dimemorfan's potential therapeutic applications beyond cough suppression, possibly in cognitive disorders.

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