Cyclic nucleotide-activated channels in carp olfactory receptor cells

Abstract

When applied from the cytoplasmic side, cyclic 3′,5′-adenosine and guanosine monophosphates reversibly increased the ion permeability of inside-out patches of carp olfactory neuron plasma membrane. The cAMP (cGMP)-induced permeability via cAMP (cGMP) concentration was fitted by Hill's equation with the exponents of 1.07 ± 0.15 (1.12 ± 0.05) and EC 50 = 1.3 ± 0.6 μ M (0.9 ± 0.3 μ M) . Substitution of NaCl in the bathing solution by chlorides of other alkali metals resulted in a slight shift of reversal potential of the cyclic nucleotide-dependent (CN) current, which indicates a weak selectivity of the channels. Permeability coefficients calculated by Goldman-Hodgkin-Katz's equation corresponded to the following relation: P Na /P K /P Li /P Rb /P Cs = 1:0.98:0.94:0.70:0.61 . Ca 2+ and Mg 2+ in physiological concentrations blocked the channels activated by cyclic nucleotides (CN-channels). In the absence of divalent cations the conductance of single CN-channels was equal to 51 ± 9 pS in 100 mM NaCl solution. Channel density did not exceed 1 μm −2. The maximal open state probability of the channel ( P o ) tended towards 1.0 at a high concentration of cAMP or cGMP. Dichlorobenzamil decreased P o without changing the single CN-channel conductance. CN-channels exhibited burst activity. Mean open and closed times as well as the burst duration depended on agonist concentration. A kinetic model with four states (an inactivated, a closed and two open ones) is suggested to explain the regularities of CN-channel gating and dose—response relations.