Acetylcholine enhances odorant sensitivity in newt olfactory receptor cells

DOI
  • Ohkuma Mahito
    Dept. of Physiol., Sch. of Med., Fujita Health Univ. Aichi, Japan
  • Kawai Fusao
    Dept. of Physiol., Sch. of Med., Fujita Health Univ. Aichi, Japan
  • Miyachi Ei-ichi
    Dept. of Physiol., Sch. of Med., Fujita Health Univ. Aichi, Japan

Bibliographic Information

Other Title
  • アセチルコリンはイモリ嗅細胞の匂い感度を修飾する

Abstract

The olfactory epithelium is innervated by efferent neurites and the olfactory receptor cells express muscarinic receptors. These observations raise the possibility that acetylcholine could affect odor responses of the olfactory receptor cells. Here we investigated the effect of acetylcholine on newt olfactory receptor cells, using the whole-cell version of the patch-clamp technique. Under current clamp condition, bath-applied 100 μM carbachol, an agonist of acetylcholine receptor, lowered spike threshold from 5.3 ± 0.6 pA to 3.8 ± 0.5 pA. Furthermore, the maximum spike frequency was increased from 9.1 ± 1.4 spikes/s to 11.0 ± 1.3 spikes/s by carbachol. These results suggest carbachol directly modulates spike generation in ORCs. Under voltage clamp, condition carbachol increased the peak amplitude of a voltage-gated T-type calcium current by 39% and sodium current by 32%. However, carbachol did not change the amplitude of an L-type calcium current or a delayed rectifier potassium current significantly. An antagonist of muscarinic acetylcholine receptor, atropine, blocked the enhancement by carbachol of sodium current, suggesting that carbachol modulates sodium current via the muscarinic receptor. Because T-type calcium current is known to lower the threshold in olfactory receptor cells, we suggest that acetylcholine, which is released from efferent fibers, may enhance odorant sensitivity by lowering the threshold of spike generation in olfactory receptor cells. [J Physiol Sci. 2006;56 Suppl:S184]

Journal

Details 詳細情報について

  • CRID
    1390282680704175616
  • NII Article ID
    130005448492
  • DOI
    10.14849/psjproc.2006.0_184_3
  • Data Source
    • JaLC
    • CiNii Articles
  • Abstract License Flag
    Disallowed

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