CYCLIC NUCLEOTIDE-ACTIVATED CHANNELS IN CARP OLFACTORY RECEPTOR-CELLS

When applied from the cytoplasmic side, cyclic 3',5'-adenosine and gua nosine monophosphates reversibly increased the ion permeability of ins ide-out patches of carp olfactory neuron plasma membrane. The cAMP (cG MP)-induced permeability via cAMP (cGMP) concentration was fitted by H ill's equation with the exponents of 1.07 +/- 0.15 (1.12 +/- 0.05) and EC50 = 1.3 +/- 0.6 muM (0.9 +/- 0.3 muM). Substitution of NaCl in the bathing solution by chlorides of other alkali metals resulted in a sl ight shift of reversal potential of the cyclic nucleotide-dependent (C N) current, which indicates a weak selectivity of the channels. Permea bility coefficients calculated by Goldman-Hodgkin-Katz's equation corr esponded to the following relation: P(Na)/P(K)/P(Li)/P(Rb)/P(Cs) = 1:0 .98:0.94:0.70:0.61. Ca2+ and Mg2+ in physiological concentrations bloc ked 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 mum-2. The maximal open state probability of the channel (P( o)) tended towards 1.0 at a high concentration of cAMP or cGMP. Dichlo robenzamil decreased P(o) without changing the single CN-channel condu ctance. CN-channels exhibited burst activity. Mean open and closed tim es 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 an d dose-response relations.