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- W1996178045 abstract "1 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. 2 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 μM) reduced the quantal content (m) without changing the quantal size (q). This effect was antagonized by naloxone (1 μM). Similar results were observed under conventional whole-cell clamp of the postsynaptic neuron. 3 A specific agonist of the μ-opioid receptor, [D-Ala2, M-Me-Phe4,Gly5]enkephalin-ol (DAMGO) reduced m without changing q. A specific agonist of the δ-opioid receptor, [d-Pen2, d-Pen5]enkephalin (DPDPE) also reduced m without changing q. 4 Both L-ENK and [Met5]enkephalin (M-ENK) reduced the stimulus-dependent increment of the intraterminal Ca2+ concentration (Δ[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 Δ[Ca2+]t more effectively than DPDPE. 5 When extracellular Ca2+ was replaced by Ba2+, the stimulus-dependent increment of the intraterminal Ba2+ concentration (Δ[Ba2+]t) was also reduced by L-ENK or DAMGO. 6 L-ENK reduced Δ[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 ω-conotoxin GVIA (ω-CgTxGVIA), the Δ[Ca2+]t was no longer sensitive to L-ENK and DAMGO. 7 It is suggested that enkephalins reduce the transmitter release through presynaptic opioid receptors. The μ-opioid receptor may suppress presynaptic Ca2+ influx by selectively inhibiting N-type Ca2+ channels." @default.
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- W1996178045 date "2000-05-01" @default.
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- W1996178045 title "μ‐Opioid receptor inhibits N‐type Ca<sup>2+</sup>channels in the calyx presynaptic terminal of the embryonic chick ciliary ganglion" @default.
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- W1996178045 doi "https://doi.org/10.1111/j.1469-7793.2000.00769.x" @default.
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