An investigation was made into the nature of the role played by the noradrenergic innervation of the pacinian corpuscle. Corpuscles of the cat mesentery and mesocolon were used in all experiments. Blockade of noradrenergic beta receptors by dichloroisoproterenol and interference with norepinephrine release by reserpine are each capable of reversibly blocking mechanoelectric transduction by the pacinian corpuscle. The monoamine oxidase inhibitors iproniazid and phenelzine are capable of protecting the transducer from the blocking effects of reserpine. It is concluded that the presence of norepinephrine, as maintained by sympathetic tonus, is required for the afferent nerve terminal of the pacinian corpuscle to be mechanosensitive.
When the sensory fiber of a Pacinian corpuscle (in cat mesentery) is transected (at the inferior mesenteric nerve) transduction fails within 30 hours: the nerve ending produces no generator potentials in response to mechanical stimulation. Electrically elicited nerve impulse conduction continues for at least another 18 hours. A transducer mechanism develops on a regenerating nerve fiber when this fiber enters the denervated corpuscle. Such transducer development takes place on myelinated fibers from the inferior mesenteric nerve, which normally supplies corpuscles, as well as on myelinated hypogastric nerve fibers, which normally do not go to corpuscles, including fibers larger than the original corpuscle afferents.
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