Unit activity in the hypothalamus and the sympathetic response to hypoxia and hypercapnia

The activity of 232 neurons in the hypothalamus and other forebrain regions was recorded with stereotaxically oriented steel microelectrodes in rabbits under light urethane anesthesia. Inhalation of N 2 or N 2O for 10 to 30 sec reduced brain oxygen tension by 30 to 90 per cent and accelerated the firing rate of 27 per cent of neurons tested. Slowing to hypoxia occurred in 36 per cent. Inhalation of 80 per cent CO 2 and 20 per cent O 2 for 5 to 15 sec elevated brain oxygen tension and 90 per cent of the neurons tested gave a response to this stimulus. In the hypothalamus thirty-one of forty-six neurons were accelerated by hypercapnia. A high proportion of tested neurons in the posterior and lateral areas of the hypothalamus were excited by hypoxia, hypercapnia and pain or auditory stimuli. In addition to the effects on neuron firing, hypoxia and hypercapnia produced a rise in arterial pressure, bradycardia and an activation of the electrocorticogram. Similar changes were elicited by electrical stimulation of the sympathetic zone of the hypothalamus. It is suggested that the cerebrovascular supply may be regulated in part by “sympathetic” neurons in the hypothalamus responsive to hypoxia or hypercapnia.