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1 Department of Pharmacology, Harvard Medical School, Boston, Massachusetts
Successive intravenous injections of nicotine cause a biphasic block of the superior cervical ganglion of the spinal cat. 1) Duriusg an initial depolarizing phase, the ganglion fails to respond to any stimulant; however, during the late, non-depolarizing phase, the ganglion responds to non-nicotinic agents at a time when there is a pronounced insurmountable type of antagonism to nicotinic agents. During this late phase of the block by nicotine, the nictitating membrane responds to preganglionic stimulation; i.e, ganglionic transmission occurs in spite of block of the nicotine receptors. At this time, there is facilitation of the ganglionic actions of muscarinic agents, and exogenous acetylcholine acts on the muscarinic receptors of the ganglion. Ganglionic transmission is likewise mediated through muscarinic receptors, since it is abolished by small doses of atropine. Furthermore, agents that reduce the effects of muscarinic ganglion stimulants during the late phase of the block by nicotine (morphine and hexamethonium) similarly reduce responses to preganglionic stimulation. It is suggested that the ganglion can transmit preganglionic impulses via muscarinic mechanisms if 1) the nicotinic receptors are blocked, and 2) the sensitivity of the muscarinic mechanisms is increased.
Submitted on April 11, 1966