Studies of the role of the central nucleus of the amygdala in controlling cardiovascular functions.

Studies on cats anesthetized with a mixture of chloralose and Nembutal addressed the effects of high-frequency stimulation (100 impulses/sec) of the central nucleus of the amygdala on bioelectrical activity in two postganglionic sympathetic nerves-the inferior cardiac nerve and the vertebral branch of the stellate ganglion, which innervate the coronary vessels and the vessels of the anterior thorax respectively. The central nucleus of the amygdala was found to have differential, selective effects, in most experiments producing increases in the amplitude of integrated activity in the inferior cardiac nerve and decreases in the amplitude of biopotentials in the vertebral nerve. In a few experiments, a second type of modulation of the activities of these two postganglionic nerves was seen, with selective inhibition of activity in the inferior cardiac nerve and an accompanying increase in activity in the vertebral nerve. Stimulation of the central nucleus of the amygdala induced significant increases in systemic arterial blood pressure. The role of the central nucleus of the amygdala in the development of experimental neurogenic hypertension was studied in a series of chronic experiments on rats; these established that rats subjected to bilateral electrolytic lesioning of the central nucleus of the amygdala prevented the development of neurogenic hypertension induced by daily imposition of stress for four weeks for induction of operant aversive conditioned reflexes, which was not the case in control rats. The role of the central nucleus of the amygdala in the regulation of vascular tone is discussed.

An investigation of certain physiological mechanisms of the neurohumoral regulation of vascular tone.

The neuronal organization of the hypothalamobulbar system of regulation of vascular tone was studied in experiments on cats anesthetized with chloralose and nembutal and immobilized by dithylin [suxamethonium iodide]. It was established that the descending influence of the posterior, tuberal, and paraventricular structures of the hypothalamus on the activity of antidromically identified sympathicoactive reticulospinal neurons of the ventrolateral region of the medulla oblongata is realized by mono-, oligo-, and polysynaptic mechanisms. It was shown in a series of experiments carried out in rats that animals subjected to chemical desympathization, by contrast with the controls, do not develop chronic neurogenic hypertension during a six-week stressor influence on higher nervous activity. The central and peripheral neurohumoral mechanisms of the regulation of vascular tone are discussed.

Neuronal and neurochemical mechanisms of hypothalamic inhibition of the nociceptive reflex.

Using cats anesthetized with chloralose-Nembutal we have studied the effect of high frequency stimulation of the medial and lateral structures of the posterior, tuberal, and anterior hypothalamus, and also of the central gray matter of the midbrain on the nociceptive jaw-opening reflex induced by tooth pulp stimulation. We recorded the EMG response of the digastric muscle as the index of the nociceptive reflex. We have shown that the EMG response of the nociceptive reflex is effectively suppressed on stimulation of all hypothalamic structures and the central gray matter, the threshold of the suppressive action being lower on stimulation of the central gray matter. The effects of the hypothalamic suppression of the nociceptive reflex were eliminated almost completely after naloxone administration, with the exception of the central gray matter, which is slightly more resistant to the action of this agent. After bilateral electrolytic destruction of the central gray matter the antinociceptive effect of the hypothalamus was retained, decreasing only insignificantly, The effect of complete suppression of the amplitude of the EMG response, similar to the effect of stimulation of the hypothalamus and the central gray matter, was also observed after intravenous administration of phenapidine, an opiate agonist with a marked central analgesic action. The neuronal and neurochemical mechanisms of hypothalamic suppression of the nociceptive jaw-opening reflex are discussed.