Long-term regulation of neurotransmitter by adrenaline

用细胞内记录技术研究了肾上腺素作用下牛蛙交感神经节烟碱型乙酰胆碱突触对递质释放的长时程增强作用。分别以低钙、高镁溶液中记录的快速兴奋性突触后电位的量子含量和高K+溶液中的微型诱发电位频率作为递质自发释放的指标。研究了两个问题：1)直接参与促进递质释放的机制和2)ADR-ltp表达的调节机制。在存在Ca^&lt；2+&gt；离子载体(A23187：10M)或Ca^&lt；2+&gt；离子载体(A23187：10M)的情况下，成对脉冲(50ms间隔)诱导的短期易化作用被降低，但不受K^+通道抑制剂(TEA：10 mM)的影响。2)TEA不影响ADR-LTP的大小，但能显著增加突触的量子含量和突触延迟。相反，在ADR-LTP期间，突触延迟没有改变。3)在ADR-LTP过程中，微型ESP出现频率增加。二丁酰环GMP(100M)与肾上腺素或DBC-AMP联合应用可抑制ADR-LTP和二丁酰环AMP(ADC-AMP：1 mM)诱导的LTP。肾上腺素(10M)作用10min以上，ADR-LTP的幅度不增加，而DBC-AMP引起的LTP则随作用时间从30min增加到1h而显著增加。这些结果提示，肾小管内钙离子基础水平升高是ADR-LTP的一种机制。因此，涉及环化GMP或B-肾上腺素能受体脱敏的两种机制似乎调节ADR-LTP的机制。

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.