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Contribution of Cyclic-Nucleotide-Gated Channels to the Resting Conductance of Olfactory Receptor Neurons

Raymund Y. K. Pun ^* and Steven J. Kleene 

^* Department of Molecular and Cellular Physiology, and Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati, Cincinnati, Ohio 45267

Correspondence: Address reprint requests to Raymund Y. K. Pun, Dept. of Molecular and Cellular Physiology, University of Cincinnati, P. O. Box 670576, Cincinnati, OH 45267-0576. Tel.: 513-558-3113; Fax: 513-558-5738; E-mail: raymund.pun{at}uc.edu.

The basal conductance of unstimulated frog olfactory receptor neurons was investigated using whole-cell and perforated-patch recording. The input conductance, measured between -80 mV and -60 mV, averaged 0.25 nS 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 0 mV, as expected for a CNG current. Under physiological conditions, gating of CNG channels contributes 0.06 nS to the resting neuronal conductance. This implies a resting cAMP concentration of 0.1–0.3 µM. A theoretical model suggests that a neuron containing 0.1–0.3 µM 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].

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