Authors: A Muñoz A LopezReal J L LabandeiraGarcia M J Guerra
Publish Date: 2003/08/29
Volume: 153, Issue: 1, Pages: 92-99
Abstract
It is classically considered that Amphetamine acts by increasing extracellular dopamine levels However some data suggest a relevant role of other neurochemical systems The striatum is of particular interest to the study of this question We have investigated the involvement of the noradrenergic and serotonergic systems and their possible interaction in the striatal responses to Amphetamine using a double behavioral and immunohistochemical approach ie changes in locomotor activity and striatal expression of Fos In normal rats Amphetamine induced locomotor hyperactivity and striatal expression of Fos Pretreatment with the α1adrenergicreceptor antagonist Prazosin or lesion of the serotonergic system significantly reduced the locomotor hyperactivity and striatal Fos expression induced by Amphetamine Administration of Prazosin to rats with serotonergic denervation did not produce any further reduction in the Amphetamineinduced locomotor hyperactivity or striatal Fos expression compared with that observed in rats with serotonergic denervation only Amphetamine did not induce a detectable increase in Fos expression in dopaminedenervated striata and elicited intense rotation towards the dopaminedenervated side This suggests that striatal dopamine release is essential in the Amphetamineinduced effects on striatal neurons However the noradrenergic system plays an important role and the serotonergic system is necessary for mediating the effects of the Amphetamineinduced noradrenergic stimulation Concurrent stimulation of dopaminergic and serotonergic receptors appears necessary to regulate Amphetamineinduced responses in the striatal neurons
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