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

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].