Hypothalamic effects on spinal reflexes and their alteration by pentobarbital

Abstract

The effects of hypothalamic stimulation on spinal cord reflexes were investigated in intact, immobilized cats and in animals under different levels of pentobarbital anesthesia. Concurrently, potentials evoked in the hypothalamus upon peripheral stimulation were studied. In immobilized and in lightly anesthetized animals, high-frequency hypothalamic stimulation usually potentiated monosynaptic and depressed polysynaptic reflexes. The effect on the former was much more consistent and reliable. In these animals peripheral nerve stimulation evoked potentials in the hypothalamus of 20- to 40-msec latency. Moderate pentobarbital anesthesia caused the diminution of hypothalamic effects on spinal cord reflexes, and the disappearance of the peripherally evoked potentials in the hypothalamus. Deepening of anesthesia abolished hypothalamic facilitation of the spinal monosynaptic reflex. Hypothalamic stimulation had little or no effect on the polysynaptic response in those animals in which it persisted. At this stage of deep anesthesia, high-voltage secondary long latency (60–160 msec) potentials were evoked in the hypothalamus upon peripheral nerve stimulation. Although the effect of anesthesia on the spinal mechanisms may account for part of the observed results, the data indicate that the effects noted are due primarily to the actions of pentobarbital in the hypothalamus. It is postulated that in the lightly anesthetized or immobilized intact animal the facilitatory brain-stem regions have a predominant effect on spinal cord reflexes, and that anesthesia (or decerebration) attenuates this facilitatory effect, thus allowing inhibitory effect of the bulbar reticular formation on the spinal cord to be shown.