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To suppress the hyperglycemic effect of malathion in rats, a smaller amount of atropine was required when the drug was injected by intraventricular (i. vent.) than s.c. Pentobarbital, but not diazepam, blocked the hyperglycemic response. The results suggest that central accumulation of acetylcholine was the mediator of the response. Since hyperglycemia was not abolished by adrenalectomy and/or hypophysectomy, a hypothesis is presented to explain how central accumulation of acetylcholine might cause hyperglycemia.

Injection of small amounts of phentolamine into the lateral ventricle of the cat abolishes the blood pressure fall, evoked by vagal stimulation, and finally converts it into a pressure rise; all other vasomotor responses tested remain unchanged. In contrast, intraventricular pentobarbitone blocks both the pressor and depressor reactions following sciatic stimulation, although the vagal hypotension is again affected first. It appears probable that the depressor neurons, reached by afferent vagus fibers, are situated at the surface of the floor of the fourth ventricle and are thus accessible to intraventricular phentolamine. These neurons are activated by a -adrenergic transmission.

Intraventricular injection of carbachol produces hyperglycemia in rats at doses which are ineffective when given subcutaneously. This effect is suppressed by intraventricular administration of small amounts of atropine, further supporting the suggestion that the effect of carbachol is due to its action on central cholinergic receptors. Carbachol-induced hyperglycemia is not abolished by adrenalectomy and hypophysectomy, or pretreatment with reserpine.