Fos immuno-positive neurons in the subthalamic nucleus following reversal of parkinsonian symptoms by antagonism of excitatory amino acid transmission in the entopeduncular nucleus of the monoamine depleted rat

Drug-induced dyskinesias are a major drawback of the dopaminergic therapies currently employed to treat Parkinson's disease. It is commonly speculated that these dyskinesias may be mediated by functional changes within the striatum. Recent research has, therefore, focused on finding new modes of therapy which will alleviate parkinsonian symptoms without directly altering neurotransmission in the striatum. It has recently been demonstrated that the behavioural symptoms observed in dopamine-depleted rodents can be alleviated by blockade of excitatory neurotransmission in the entopeduncular nucleus. A series of experiments was conducted in order to determine whether this manipulation affected the pattern of Fos immunoreactivity in the basal ganglia elicited by dopamine depletion. The results demonstrated that the most striking change in Fos levels was found in the subthalamic nucleus, indicating that reversal of parkinsonian symptoms in this manner cannot be considered as a simple redress in the balance of activity in the output structures of the basal ganglia.