Acetylcholine enhances odorant sensitivity in newt olfactory receptor cells
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- Ohkuma Mahito
- Dept. of Physiol., Sch. of Med., Fujita Health Univ. Aichi, Japan
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- Kawai Fusao
- Dept. of Physiol., Sch. of Med., Fujita Health Univ. Aichi, Japan
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- Miyachi Ei-ichi
- Dept. of Physiol., Sch. of Med., Fujita Health Univ. Aichi, Japan
Bibliographic Information
- Other Title
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- 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
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- Proceedings of Annual Meeting of the Physiological Society of Japan
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Proceedings of Annual Meeting of the Physiological Society of Japan 2006 (0), 184-184, 2006
PHYSIOLOGICAL SOCIETY OF JAPAN
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Details 詳細情報について
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- CRID
- 1390282680704175616
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- NII Article ID
- 130005448492
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- Data Source
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- JaLC
- CiNii Articles
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- Abstract License Flag
- Disallowed