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

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Abstract

In a previous study by the authors (see record 1980-27512-001), rats were shown to have decreased locomotor and investigatory exploration after bilateral microinjections of 6-hydroxydopamine (6-OHDA) into the anterolateral hypothalamus. Theses deficits correlated with the loss of catecholamine (CA) terminals in neocortical, limbic, and anteromedioventral striatal brain sites. To test whether this correlation was causal, central CAs were increased in 2 experiments with male Sprague-Dawley rats by the ip injection of levodopa (10-40 mg/kg) after inhibition of extracerebral levo-amino-acid decarboxylase. Such treatment repaired the deficits in locomotor exploration and investigation in 6-OHDA Ss. Pretreatment with the CA antagonist chlorpromazine (1-2 mg/kg) blocked the increase in locomotor exploration and investigation produced by levodopa in 6-OHDA Ss. Results suggest, but do not prove, that levodopa produced these behavioral effects by increasing central CAs at the denervated CA receptor sites in the forebrain. Data are complementary evidence for the hypothesis that forebrain CA synaptic action is necessary for normal exploratory behavior. (22 ref) (PsycINFO Database Record (c) 2006 APA, all rights reserved)

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