Long-term regulation of neurotransmitter by adrenaline

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Long-term potentiation of transmitter release induced by the action of adrenaline (adr.-ltp) was studied in the nicotinic acetylcholine synapse of the bullfrog sympathetic ganglion, using an intracellular recording technique. The quantal content of the fast excitatory postsynaptic potentials (epsp) recorded in a low Ca^<2+>, high Mg^<2+> solution and the frequency of miniature e.p.s.ps in a high K^+ solution was used as indicators of impulse-induced and spontaneous release of transmitter, respectively. Two problems were investigated 1) a mechanism directly involved in the enhancement of transmitter release and 2) regulatory mechanisms for expression of adr.-ltp.The short-term facilitation induced by paired pulses (50 ms interval) was reduced in the presence of a Ca^<2+> chelator (quin-2/AM: 5 M) or a Ca^<2+> ionophore (A23187: 10 M) and during adr.-ltp, but unaffected by a K^+ channel inhibitor (TEA: 10 mM). 2) The magnitude of adr.-ltp was unaffected by TEA which increased markedly the quantal content and synaptic delay. In contrast synaptic delay was not altered during adr.-ltp. 3) Frequency of miniature epsp was increased during adr.-ltp. adr.-ltp and a ltp induced by dibutyryl cyclic AMP (adc-AMP: 1 mM) were suppressed by the coapplication of dibutyryl cyclic GMP (100 M) and adrenaline or dbc-AMP. The magnitude of adr.-ltp was not enhanced by increasing the duration of application of adrenaline (10 M) for more than 10 min, while the ltp induced by dbc-AMP was auqumented markedly by increasing the time of ap-plication from 30 min to 1 hr. These results suggest that an increase in the basal level of the intraterminal Ca^<2+> is a mechanism of adr.-ltp. Thus, two mechanisms involving cyclic GMP or desensitization of B-adrenoceptor appear to regulate the mechanism of adr.-ltp.