Mechanisms regulating the adrenaline-induced long-term potentiation in bullfrog sympathetic ganglia.

Two regulatory mechanisms on the long-term potentiation of transmitter release induced by adrenaline (adr.-l.t.p.) in bullfrog sympathetic ganglia were studied by recording intracellularly the fast excitatory postsynaptic potentials. An increase in exposure time to adrenaline from 10 min to 60 min did not enhance the magnitude of adr.-l.t.p. However, increasing an exposure time to dibutyryl cyclic AMP (1 mM) up to 60 min progressively enhanced the magnitude of the nucleotide-induced potentiation, indicating the desensitization of the beta-adrenoceptor. The desensitization remained at 20 min after the removal of adrenaline in all the five cells but disappeared at 60-90 min in four cells out of eight. Under the latter condition, the second l.t.p. was summated on the first one. Dibutyryl cyclic GMP (100 microM) blocked the generation of the l.t.p. induced by dibutyryl cyclic AMP (1 mM) as well as that of adr.-l.t.p. Muscarine (10 microM) or adenosine (1 mM), a possible candidate for raising intraterminal cyclic GMP, did not significantly affect adr.-l.t.p. These results suggest that adr.-l.t.p. is regulated by the desensitization of beta-adrenoceptor and a process which involves endogenous cyclic GMP acting on a step subsequent to the cyclic AMP production.