THE INFLUENCE OF HYPOTHALAMIC STIMULATION ON CORTICALLY INDUCED MOVEMENTS AND ON ACTION POTENTIALS OF THE CORTEX

Abstract

Simultaneous stimulation of the hypothalamus (sub-threshold for somatic reactions) and of the motor cortices (cat, monkey) results in intensification of motor discharge in the peripheral musculature. This intensification is expressed as decrease in the period of latency of response, increase in magnitude of movements through the same joints activated during cortical stimulation alone, spread of motor discharge, contralaterally and ipsilaterally, and the evocation of muscular contractions when a sub-threshold stimulus is applied to the cortex. Those areas in the hypothalamus which are productive of a facilitatory effect are likewise productive of a sympathetic autonomic effect. Facilitation, however, is independent of sympathetic discharge; indeed, elimination of sympathetic pathways to the brain intensifies the facilitatory effect. Both cortices (ipsilateral and contralateral) are under the influence of the hypothalamus of one side of the brain. Generally speaking, wherever a motor response is obtainable from the cortex, facilitation can be found as well. The optimal area in the basal forebrain concerned with this function is the posterior hypothalamus, but such potentiality is not restricted here. Since hypothalamic facilitation of the cortically induced motor response persists after a small cor- tical area has been isolated from adjacent parts of the cortex, the intensification of the response is not due to functional spread to other parts of the motor cortex. Stimulation of the hypothalamus results in a distinctive, enduring excitatory effect on the cerebral cortex, as manifested by increased rate and amplitude of discharge in the spontaneous electrocortico-gram and in suppression of "Dial" potentials during and following hypothalamic stimulation. Firing of cortical neurons initiated by local application of strychnine is likewise increased in frequency as a result of hypothalamic excitation. This facilitatory influence resultant from stimulation of the hypothalamus is found in motor and in primary sensory receptive and association areas as well. It is bilateral in nature, but most marked ipsilateral with the site of hypothalamic stimulation. The nuclear areas in the basal forebrain responsive with such an effect are likewise productive of sympathetic autonomic phenomena. The changes are independent of sympathetic autonomic phenomena as such and persist after elimination of the adrenals. The alteration in the electrocorticogram is thought to be due to increased frequency of discharge of cortical ganglion cells, as a consequence of a lesser degree of synchrony of discharge, and firing of a greater number of neurons than those responsible for the normal electrocorticogram. The fact that hypothalamic potentials following stimulation recorded from the stimulated area are unchanged while increased cortical potentials persist indicates that the changes in the e.c.g. are only initiated by hypothalamic impulses but are self-sustained at the cortical level. The complete parallelism between the two sets of experiments summarized above suggests as one important site of hypothalamic facilitation of the pyramidal system the sensori-motor cortex. Hypothalamic cortical facilitation may be responsible for the overcoming of paralysis under conditions of emotional stress and possibly for the initiation of epileptic seizures as well. The exptl. finding that cortical activity in sensory projection and association areas is likewise altered as a result of hypothalamic stimulation indicates that hypothalamic cortical facilitation is not restricted to the motor system.