Serotonergic innervation of the foot of the pond snail Lymnaea stagnalis (L.).

The aminergic innervation of the foot of Lymnaea stagnalis was investigated using electron microscopy, immunocytochemistry, and HPLC. The foot was found to contain large amounts of serotonin and dopamine, though at lower concentrations than are found in nervous tissue. Serotonin containing tissue was concentrated in the ventral surface of the foot, under ciliated areas of the epidermis where it occurred in varicosities, with fine tracts joining these varicosities. Varicosities also occurred in deeper tissues, probably adjacent to mucus cells. Positive fluorescence for serotonin in axons was found in nerves innervating the foot, but few neuronal cell bodies containing serotonin were detected, indicating that most of the innervation was coming from the central ganglia. Axon varicosities were found using TEM on ciliated cells, mucus cells, and muscle cells as well as interaxonal junctions (possibly non-synaptic) within nerves. The neuronal varicosities contacting the ciliated cells and mucus cells contained mostly dense-cored vesicles of between 60 and 100 nm in diameter. Smaller, lucent vesicles also occurred in these terminals. The origin and significance of this innervation is discussed. It is suggested that both serotonin and dopamine may play a large role in controlling ciliary gliding by the foot.

An investigation of the mechanism involved in the cholinergic action of meptazinol.

In concentrations above 20 microM, (+/-)-meptazinol produced a contraction of the guinea-pig isolated ileum and this effect was antagonized by atropine (0.01 to 0.3 microM) in a manner which was not competitive. Cooling the preparation to 15 degrees C blocked the contractile action of meptazinol and of dimethylphenylpiperazinium (DMPP) but did not affect the action of carbachol. Twitch responses of the rat phrenic nerve-diaphragm preparation induced by indirect electrical stimulation in the presence of naloxone (20 nM) were potentiated by meptazinol (1 to 40 microM) which also reversed a partial blockade of the twitch induced by tubocurarine. Neither of these effects was seen in tissues which had been pretreated with the cholinesterase inhibitor BW284C51 (0.2 microM) though tetraethylammonium iodide (40 microM) was still able to enhance the responses to stimulation. In the presence of naloxone (20 nM) electrically induced responses of the rat isolated rectum were abolished by cinchocaine (10 microM), partially blocked by atropine (0.1 to 0.4 microM) and potentiated by meptazinol (1 to 30 microM). The latter action was not seen when meptazinol was administered in the presence of BW284C51. It is concluded that the cholinergic action of meptazinol in these tissues is due to an indirect effect, probably involving inhibition of cholinesterase and that no evidence was seen of any ability to increase the release of acetylcholine itself.