A vertebrate model system has been established where the Ca2+ current, the Ca2+ concentration and the transmitter release were measured from an identified giant presynaptic terminal of chick ciliary ganglion. We have investigated the inhibitory mechanisms in the presynaptic terminal of neuromodulators. The synaptic transmission was suppressed by ATP and its metabolite adenosine. Both the transmitter release and the nerve-evoked increase of Ca2+ in the presynaptic terminal were suppressed by the activation of Al-adenosine autoreceptors. When the ganglion was pretreated by ω-conotoxin GVIA (ω-CgTx), the reduction of Ca2+ influx was not observed. It is concluded that the suppression of ω-CgTx-sensitive subtype of presynaptic Ca2+ channels through Al-adenosine receptors is responsible for the suppression of Ca2+ influx and resultant inhibition of transmitter release. We have examined other inhibitory neuromodulators, opioids and noradrenaline. The results implicate the general view of presynaptic modulation that various receptors are targeting various sites of action although some sites are targeted by multiple receptors. The ω-CgTx-sensitive Ca2+ channel is one of the final common sites of modulation.
|Number of pages||8|
|Issue number||SUPPL. 1|
|Publication status||Published - 1994 Nov 8|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)