Specific features of sensorimotor cerebral cortex activity modulation by dopamine releaser amantadine

Abstract

The modulatory effects of amantadine (1-adamantanamine) on the activity of sensorimotor cerebral cortex neurones during microiontophoretic application of agonists of glutamatergic and GABA-ergic (gamma-aminobutyric acid) transmission were studied. In non-anaesthetised cats, dopamine (DA) released by amantadine application in a small area of the neocortex increased baseline and evoked neuronal activity, providing stabilization and optimum course of both the neuronal and the conditioned responses of the animal. Amantadine eliminates a decrease in the level of neuronal baseline and evoked activity and marked increase in the latency of neuronal activation and conditioned movement mediated by D2 receptor antagonist sulpiride ((S)-5-aminosulfonyl-N-[(1-ethyl-2-pyrrolidinyl) methyl]-2-methoamantadineybenzamide) or GABA. This is reflected by a proportionate decrease in the onset of neuronal impulse reaction and latency of conditioned movement. Combined NMDA (N-methyl-D: -aspartate) and amantadine application also caused a considerable increase in baseline and evoked activity, but produced a slightly weaker effect than that evoked by NMDA application alone. A decrease in the baseline and evoked neuronal activity after NMDA withdrawn lasted during next control session (up to 40 min). The ability of DA releaser amantadine to alleviate significant increase in the latency of neuronal responses and conditioned movement induced by sulpiride or GABA suggests that dopamine modulates the activity of GABA-ergic inhibitory fast spike interneurons in the cat sensorimotor cortex during conditioning.