The effect of intracranial stimulation on the chronically denervated nictitating membrane of the encéphale isolé cat has been studied. After eliminating sympathoadrenal discharge, we found that the nictitating membrane responds to direct stimulation of the brain stem and certain cranial nerves through: 1) an intrinsic sensitivity to direct mechanical stimulation which develops in the smooth-muscle fibers of the nictitating membrane after chronic denervation; 2) an effect by way of the greater superficial petrosal nerve, producing retraction of the nictitating membrane from diffusion of acetylcholine onto the sensitized smooth muscle from secretomotor fibers innervating nearby orbital glands; and 3) finally, after exclusion of cranial nerve effects, one can still, under optimal conditions, obtain retraction of the nictitating membrane after stimulation of the reticular formation, an effect that is tentatively ascribed to the release of a humoral factor from some intracranial source. The bearing of these findings on previous work in which the nictitating membrane has been used as an indicator of circulating neurohumors is discussed.
Previous work has suggested that catecholamines might function as transmitter substances in portions of the reticular activating system. In this study, we used classical autopharmacological methods in an effort to detect catecholamine release into the systemic circulation of the encéphale isolé preparation during stimulation of the reticular formation. Fluctuations of blood pressure and movements of the denervated nictitating membrane were observed after exclusion of effects mediated by the cranial nerves and sympathoadrenal discharge. Since these effects were not blocked by Dibenzyline, and could be reproduced by small doses of Pitressin, they were ascribed to the release of vasopressin from the neurohypophysis rather than to catecholamine release. Some preliminary data were obtained on the localization in the midbrain of a pathway that appears to influence the hypothalamoneurohypophysial system, and that may possibly be responsible for the antidiuretic effects of pain and emotional excitement.
Thresholds for pentylenetetrazol-induced seizures were determined in cats after varying periods of deep barbiturate intoxication. Thresholds measured 18 to 22 hours after the last dose of barbiturate were significantly decreased even with the shortest period of barbiturate intoxication employed (26 hr). This decrease was interpreted as a manifestation of barbiturate withdrawal. Spontaneous seizures were seen during the withdrawal period after as little as 2 weeks of intoxication. The time course of the development of physical dependence was compared to the time course of the development of denervation supersensitivity in peripheral structures.
