Abstract
The intravenous injection of 0.05 to 2.5 mg. of morphine reduced the response of the nictitating membrane in the cat to pre- and post-ganglionic stimulation. This inhibitory action of morphine was due neither to inhibition of ganglionic transmission nor to a depressant action on the smooth muscle of the nictitating membrane. It is suggested that morphine inhibits the release of the sympathetic transmitter from the postganglionic nerve endings.
Small amounts of morphine (5 to 20 μg.) injected intravenously reduced or abolished the contraction of the nictitating membrane due to the injection of histamine, pilocarpine and 5-HT into the arterial blood supply of the superior cervical ganglion. This inhibitory action of morphine was due to an action on the ganglion cells, since such small amounts of morphine did not reduce the response of the nictitating membrane to postganglionic stimulation. Similar amounts of morphine did not abolish the stimulation of the ganglion by nicotine, tetramethylammonium and potassium chloride.
The results provide further evidence for the view that histamine, pilocarpine, and 5-hydroxytryptamine have no “nicotine-like” properties but act on receptors of the ganglion cells different from the acetylcholine receptors.
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Selected References
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