Hyper-running activity originating from the hypothalamus : An element of instinctive behaviors

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We found that excitation of neurons in the ventromedial nucleus of the hypothalamus(VNM)induced stereotyped hyper-running, which was not associated with the motivation of an attack or escape. Such running activity is regarded as one of the principal elements of instinctive behaviors. Then it is presumed that stereotyped metabolic changes accompany the running activity. In this study, neurnal mechanisms in the VMH involved in inducing the hyper-running and in changing glucose metabolism were investigated.The injection of polymer-gel into the VMH was shown to induce the hyper-running. This was probably due to disinhibition of the GABAergic inhibitory neuronal system, since inclusion of GABA in the gel failed to induce the running activity. Injection of kainate into the VMH also induced the hyper-running ; the effect of kainate was not blocked by GABA. These findings suggest that neuroexcitatory amino acids acting at the kainate receptor in the VMH play a physiological role in inducing Junning activity and that the release of such amino acids are presynaptically inhibited by GABAergic neurons.Injection of kainate into the VMH increased plasma levels of corticosterone, epinephrine, norepinephrine and glucose, as well as inducing the hyper-running. This suggests that kainate receptors in the VMH are also involved in evoking metabolic changes required to maintain running activity.It is also suggested in the present study that the neuronal pathway via the marmmillary body and the midbrain central gray is involved in the VMH-inducing running activity and that neuronal output from the VMH affects the circadian locomotor activity.