| 10790157 |
Endo K, Yawo H: mu-Opioid receptor inhibits N-type Ca2+ channels in the calyx presynaptic terminal of the embryonic chick ciliary ganglion. J Physiol. 2000 May 1;524 Pt 3:769-81.
A study was made on the mechanisms by which enkephalins inhibit synaptic transmission at calyx-type presynaptic terminals in the ciliary ganglion of chick embryos at stages 39-40. Excitatory postsynaptic currents (EPSCs) were recorded by nystatin-perforated patch clamp at low [Ca2+] o and high [Mg2+] o. [Leu5] enkephalin (L-ENK, 1-10 microM) reduced the quantal content (m) without changing the quantal size (q). This effect was antagonized by naloxone (1 microM). Similar results were observed under conventional whole-cell clamp of the postsynaptic neuron. A specific agonist of the mu-opioid receptor, [D-Ala2, M-Me-Phe4,Gly5] enkephalin-ol (DAMGO) reduced m without changing q. A specific agonist of the delta-opioid receptor, [d-Pen2, d-Pen5] enkephalin (DPDPE) also reduced m without changing q. Both L-ENK and [Met5] enkephalin (M-ENK) reduced the stimulus-dependent increment of the intraterminal Ca2+ concentration (Delta [Ca2+] t) without affecting the decay time constant of the intraterminal Ca2+ concentration and basal Ca2+ level. This effect was antagonized by naloxone. DAMGO reduced Delta [Ca2+] t more effectively than DPDPE. When extracellular Ca2+ was replaced by Ba2+, the stimulus-dependent increment of the intraterminal Ba2+ concentration (Delta [Ba2+] t) was also reduced by L-ENK or DAMGO. L-ENK reduced Delta [Ca2+] t even in the presence of 4-aminopyridine (4-AP), which blocks the transient K+ conductance during the falling phase of the presynaptic action potential. When N-type Ca2+ channels were blocked by omega-conotoxin GVIA (omega-CgTxGVIA), the Delta [Ca2+] t was no longer sensitive to L-ENK and DAMGO. It is suggested that enkephalins reduce the transmitter release through presynaptic opioid receptors. The mu-opioid receptor may suppress presynaptic Ca2+ influx by selectively inhibiting N-type Ca2+ channels. |
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