Some neurones are endowed with receptors for endorphins and narcotic analgesics. Activation of these receptors results in a depression of the release of transmitter per impulse. It is currently believed that narcotic analgesics and endorphins depress the stimulus-induced influx of calcium (Ca2+) into the terminal and thereby modify the amount of the ion which triggers the release of the transmitter from intracellular stores. The influx of Ca2+ is largely governed by the Ca2+ "channel", which opens during depolarization of the neuronal membrane either after an action potential (electrical stimulus) or in the presence of high extracellular potassium (K+) or nicotinic stimulants (chemical stimulus). The evoked influx of Ca2+ can be affected by a direct action on the Ca2+ "channel" or by primary actions on other membrane properties that subsequently regulate the Ca2+ "channel". In many tissues narcotic analgesics and endorphins fail to inhibit transmitter release. This may be accounted for by the possibility that either such neurones lack presynaptic opiate receptors or that the function of existing receptors remains latent under the experimental conditions employed. Currently, there is insufficient evidence for endorphins physiologically modulating transmitter release.
Analgesics, Opioid Calcium