Contribution of cyclic-nucleotide-gated channels to the resting conductance of olfactory receptor neurons.
Contribution of cyclic-nucleotide-gated channels to the resting conductance of olfactory receptor neurons.
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环核苷酸门控通道对嗅觉受体神经元静息电导的贡献。
DOI:
10.1016/s0006-3495(03)70064-2
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发表时间:
2003
期刊:
影响因子:
--
通讯作者:
Kleene,StevenJ
中科院分区:
文献类型:
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作者:
Pun,RaymundYK;Kleene,StevenJ
The basal conductance of unstimulated frog olfactory receptor neurons was investigated using whole-cell and perforated-patch recording. The input conductance, measured between −80mV and −60mV, averaged 0.25nS in physiological saline. Studies were conducted to determine whether part of the input conductance is due to gating of neuronal cyclic-nucleotide-gated (CNG) channels. In support of this idea, the neuronal resting conductance was reduced by each of five treatments that reduce current through CNG channels: external application of divalent cations or amiloride; treatment with either of two adenylate cyclase inhibitors; and application of AMP-PNP, a competitive substrate for adenylate cyclase. The current blocked by divalent cations or by a cyclase inhibitor reversed near 0mV, as expected for a CNG current. Under physiological conditions, gating of CNG channels contributes ∼0.06nS to the resting neuronal conductance. This implies a resting cAMP concentration of 0.1–0.3μM. A theoretical model suggests that a neuron containing 0.1–0.3μM cAMP is poised to give the largest possible depolarization in response to a very small olfactory stimulus. Although having CNG channels open at rest decreases the voltage change resulting from a given receptor current, it more substantially increases the receptor current resulting from a given increase in [cAMP].