Long-term regulation of neurotransmitter by adrenaline

肾上腺素（adr.-）作用引起的递质释放的长时程增强用细胞内记录技术研究了牛蛙交感神经节烟碱乙酰胆碱突触的LTP。在低Ca^2+、高Mg^2+溶液中记录的快速兴奋性突触后电位（epsp）的量子含量和在高K^+溶液中记录的微型e.p.s.ps的频率分别被用作冲动诱导和自发释放递质的指标。研究了两个问题：1）直接参与递质释放增强的机制和2）adr表达的调节机制。在Ca^2+螯合剂（quin-2/AM：5 M）或Ca^2+离子载体（A23187：10 M）存在下，以及在adr. ltp，但不受K^+通道抑制剂（TEA：10 mM）的影响。2)adr的大小- TEA显著增加量子含量和突触延迟，对ltp无影响。相反，在adr过程中突触延迟没有改变。ltp 3)adr时微小epsp频率增高ltp adr.-双丁酰环磷酸鸟苷（100 μ M）和肾上腺素或dbc-AMP共同作用可抑制由双丁酰环磷酸腺苷（adc-AMP：1 mM）诱导的ltp和a ltp。adr的大小-肾上腺素（10 M）作用10分钟以上，对ltp无明显增强作用，而dbc-AMP作用30分钟至1小时，对ltp有明显增强作用。ltp因此，涉及环GMP或B-肾上腺素受体脱敏的两种机制似乎调节adr. ltp

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.