An opioid mechanism modulates central and not peripheral dopaminergic control of ciliary activity in the marine mussel Mytilus edulis.
Opioid receptors and enkephalinergic neurons in the central nervous system of Mytilus edulis have been reported. Also known is that the lateral epithelium of the gill is innervated by serotonergic, cilioexcitatory neurons and dopaminergic, cilioinhibitory neurons. The aim of the present report is to look for an effect of opioid agonists on the nervous control of the lateral cilia. Dopamine applied to the cerebral ganglion inhibited the activity of lateral cilia in the gill. This effect was blocked by the application of several opioids to the visceral ganglion. The block was reversed by the application of naloxone to the visceral ganglion. Dopamine applied to the visceral ganglion also inhibited lateral ciliary activity as shown earlier. Opioids applied to the visceral ganglion partially blocked this effect but this was overcome by higher concentrations of dopamine. Preparations with low endogenous rates of ciliary beating were stimulated by the application of opioids to the visceral ganglion. Naloxone blocked this effect. Preparations with high endogenous rates of ciliary beating were inhibited by the application of naloxone to the visceral ganglion. Electrical stimulation of the cerebrovisceral connective produced excitatory and inhibitory effects depending on the rate of stimulation. Morphine applied to the visceral ganglion diminished the cilioinhibitory effects and enhanced the cilioexcitatory effects of electrical stimulation. Morphine applied to the gill had no effect on the cilioinhibitory action of dopamine applied to the visceral ganglion. There was no observable effect of opioids applied to the gill and no alteration in the cilioinhibitory effect of dopamine or the cilioexcitatory effect of serotonin applied directly to the gill in the presence of opioids. Specific opioid binding sites were found in the visceral ganglion but were not found in gill, palp, mantle, or visceral mass tissue. A dopamine-stimulated adenylate cyclase activity was again found in the visceral ganglion and the gill. Etorphine reduced the dopamine stimulation of cyclase in the ganglion but not in the gill. It is postulated that a cilioinhibitory, dopaminergic mechanism includes nerves running from the cerebral ganglion to the gill with synaptic transmission in the visceral ganglion that can be modulated by opioids.
D000818:Animals; D049872:Bivalvia; D002490:Central Nervous System / Q000166:cytology / Q000187:drug effects; D002923:Cilia / Q000187:drug effects / Q000502:physiology; D004298:Dopamine / Q000502:physiology*; D004723:Endorphins / Q000378:metabolism / Q000502:physiology*; D004744:Enkephalin, Methionine / Q000031:analogs & derivatives / Q000494:pharmacology; D005048:Etorphine / Q000494:pharmacology; D005724:Ganglia / Q000166:cytology / Q000187:drug effects; D005880:Gills / Q000166:cytology / Q000187:drug effects / Q000294:innervation*; D011957:Receptors, Opioid / Q000187:drug effects / Q000378:metabolism
D004723:Endorphins; D011957:Receptors, Opioid; D005048:Etorphine; D004744:Enkephalin, Methionine; C022118:enkephalinamide-Met, Ala(2)-; D004298:Dopamine