Effects of interruption of the nigrostriatal pathway and of dopaminergic agents on the spontaneous activity of globus pallidus neurons in the awake monkey.
Interruption of the nigrostriatal pathway has been shown to change parameters of striatal activity. These changes are often difficult to explain because the functional structure of the striatum is not understood sufficiently. The function of the globus pallidus appears to be simpler. It transmits the output of the striatum to the thalamus and to the midbrain. Yet the effects of interruption of the nigrostriatal pathway on the activity of pallidal neurons are unknown. To study these effects the spontaneous activity of globus pallidus neurons was recorded in intact monkeys and in monkeys with lesions of the ventromedial midbrain tegmentum. The two groups of animals were studied with and without administration of dopaminergic agents. In intact monkeys medial pallidal neurons discharge uninterruptedly at high firing rates, while the discharge of most lateral pallidal neurons is interrupted by relatively long periods of silence. Lesions involving the nigrostriatal pathway change the firing patterns but not the mean firing rates of pallidal neurons. In lesioned monkeys pallidal neurons fire in bursts continuously: during movement, rest and sleepiness. Two lines of evidence strongly suggest that the bursting pallidal activities are a consequence of the interruption of the nigrostriatal dopaminergic pathway: (1) the percentage of bursting pallidal neurons is proportional to the amount of degeneration in the pars compacta of the ipsilateral substantia nigra; (2) chronic administration of dopamine antagonists, haloperidol and reserpine, reproduces in intact monkeys the bursting activities observed in lesioned animals. On the other hand, single injections of dopamine agonists, apomorphine and piribedil, silence the medial pallidum and concomittantly abolish the signs of parkinsonism displayed by lesioned monkeys.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology*; D003342:Corpus Striatum / Q000187:drug effects / Q000502:physiology*; D005071:Evoked Potentials / Q000187:drug effects; D005917:Globus Pallidus / Q000187:drug effects / Q000502:physiology*; D006220:Haloperidol / Q000494:pharmacology; D000882:Haplorhini; D006246:Harmaline / Q000494:pharmacology; D008253:Macaca mulatta; D009068:Movement; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D010300:Parkinson Disease / Q000503:physiopathology; D010879:Piperazines / Q000494:pharmacology*; D010891:Piribedil / Q000494:pharmacology*; D012110:Reserpine / Q000494:pharmacology; D013378:Substantia Nigra / Q000187:drug effects / Q000502:physiology*
D010879:Piperazines; D012110:Reserpine; D006246:Harmaline; D010891:Piribedil; D006220:Haloperidol; D001058:Apomorphine