L-dopa repairs deficits in locomotor and investigatory exploration produced by denervation of catecholamine terminal fields in the forebrain of rats.

Abstract

Rats had decreased locomotor and investigatory exploration after bilateral microinjections of 6-hydroxydopamine into the anterolateral hypothalamus. These deficits correlated with the loss of catecholamine terminals in neocortical, limbic and anteromedioventral striatal brain sites. To test whether this correlation was causal, central catecholamines were increased by the i.p. administration of L-dopa (10-40 mg/kg) after inhibition of extracerebral L-amino acid decarboxylase. Such treatment repaired the deficits in locomotor exploration and investigation in 6-hydroxydopamine rats. Pretreatment with the catecholamine antagonist chlorpromazine (1-2 mg/kg) blocked the increase in locomotor exploration and investigation produced by L-dopa in 6-hydroxydopamine rats. L-dopa may have produced these behavioral effects by increasing central catecholamines at the denervated catecholamine receptor sites in the forebrain. Forebrain catecholamine synaptic action may be necessary for normal exploratory behavior.