Acetylcholine enhances excitability by lowering the threshold of spike generation in olfactory receptor cells.
Olfactory perception is influenced by behavioral states, presumably via efferent regulation. Using the whole cell version of patch-clamp recording technique, we discovered that acetylcholine, which is released from efferent fibers in the olfactory mucosa, can directly affect the signal encoding in newt olfactory receptor cells (ORCs). Under current-clamp conditions, application of carbachol, an acetylcholine receptor agonist, increased the spike frequency of ORCs and lowered their spike threshold. When a 3-pA current to induce near-threshold depolarization was injected into ORCs, 0.0 spikes/s were generated in control solution and 0.5 spikes/s in the presence of carbachol. By strong stimuli of injection of a 13-pA current into ORCs, 9.1 and 11.0 spikes/s were generated in control and carbachol solutions, respectively. A similar result was observed by bath application of 50 μM acetylcholine. Under voltage-clamp conditions, carbachol increased the peak amplitude of a voltage-gated sodium current by 32% and T-type calcium current by 39%. Atropine, the specific muscarinic receptor antagonist, blocked the enhancement by carbachol of the voltage-gated sodium current and T-type calcium current, suggesting that carbachol increases those currents via the muscarinic receptor rather than via the nicotinic receptor. In contrast, carbachol did not significantly change the amplitude of the L-type calcium current or the delayed rectifier potassium current in the ORCs. Because T-type calcium current is known to lower the threshold in ORCs, we suggest that acetylcholine enhance excitability by lowering the threshold of spike generation in ORCs via the muscarinic receptor.
Department of Physiology, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Mahito
M
Ohkuma
Fusao
F
Kawai
Ei-ichi
E
Miyachi
D000109:Acetylcholine / Q000494:pharmacology*; D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000378:metabolism; D020747:Calcium Channels, T-Type / Q000378:metabolism; D002217:Carbachol / Q000494:pharmacology; D018680:Cholinergic Antagonists / Q000494:pharmacology; D018727:Muscarinic Antagonists / Q000494:pharmacology; D018034:Olfactory Receptor Neurons / Q000187:drug effects / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism; D012455:Salamandridae; D061566:Voltage-Gated Sodium Channels / Q000378:metabolism
D020746:Calcium Channels, L-Type; D020747:Calcium Channels, T-Type; D018680:Cholinergic Antagonists; D018727:Muscarinic Antagonists; D024661:Potassium Channels, Inwardly Rectifying; D061566:Voltage-Gated Sodium Channels; D001285:Atropine; D002217:Carbachol; D000109:Acetylcholine
action potential; muscarinic receptor; patch clamp; voltage-gated current