The central action of the peptide of intestinal tract, glucagon, was studied in Albino Swiss mice (20-25 g) and Wistar rats (200-220 g). Glucagon was injected intracerebroventricularly (icv) at the dose of 0.25, 0.5 and 1 microgram in 1 microliter of distilled water per mouse or 5 micrograms in 5 microliters per rat. It was found that glucagon administered icv increased glucose content in the peripheral blood serum. Behavioral studies have shown that glucagon diminished spontaneous locomotor activity in rats and mice, impaired exploratory activity and reduced amphetamine-induced hyperactivity. The results were not dependent on hyperglycaemia because the administration of 20% glucose solution po did not cause above effects. In addition, glucagon potentiated cataleptogenic effects of haloperidol. Icv injection of glucagon did not change the pain sensitivity or seizure susceptibility. The substance did not show the anxiolytic properties and did not affect the duration of hexobarbital-induced sleep. In biochemical studies it was found that glucagon injected icv induced the decrease in GABA content while the DA content was increased. The utilization of DA was not changed. The obtained results indicated, that glucagon injected icv exerted the central action, which was manifested by the central regulation of glucose level in the periphery. Moreover, glucagon inhibited the locomotor and exploratory activity as well as the amphetamine-induced hyperactivity and enhanced haloperidol-induced catalepsy. These effect could be connected with the inhibition of the central dopaminergic structures by glucagon.