Increased behavioral response to dopaminergic stimulation of the subthalamic nucleus after nigrostriatal lesions
Identifieur interne : 000A99 ( Main/Exploration ); précédent : 000A98; suivant : 000B00Increased behavioral response to dopaminergic stimulation of the subthalamic nucleus after nigrostriatal lesions
Auteurs : Arpesh Mehta [États-Unis] ; Kyriaki Thermos [Grèce] ; Marie Rançoise Chesselet [États-Unis]Source :
- Synapse [ 0887-4476 ] ; 2000-09-15.
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Abstract
Local infusions of the nonselective dopaminergic agonist apomorphine into the subthalamic nucleus of rats has been shown to elicit orofacial dyskinesia which can be blocked by D1 but not D2 receptor antagonists. In the present study, we show that the selective D1 agonist A77636 also induces orofacial dyskinesia when injected into the subthalamic nucleus of awake rats, thus confirming a role for D1 receptors in this effect. We also examined the dyskinesia induced by intrasubthalamic injections of apomorphine in rats with an ipsilateral lesion of the nigrostriatal pathway. The orofacial response to local administration of apomorphine (1.0 μg) into the subthalamic nucleus was markedly increased in the lesioned rats. As in control rats, the enhanced behavioral response seen in lesioned rats was blocked by peripheral administration of D1 antagonists. Although D1 receptor binding autoradiography revealed no difference in D1 receptor binding in the subthalamic nucleus on the side of the lesion compared to controls, D1 binding was higher in the subthalamic nucleus on the side of the lesion compared to the contralateral side. The increased behavioral response observed after unilateral dopamine denervation suggests that the subthalamic nucleus is tonically regulated by dopaminergic projections from the substantia nigra. Furthermore, the data suggest that subthalamic D1 receptors may be involved in the development of dyskinesia induced by dopaminergic drugs. Synapse 37:298–307, 2000. © 2000 Wiley‐Liss, Inc.
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DOI: 10.1002/1098-2396(20000915)37:4<298::AID-SYN7>3.0.CO;2-A
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In the present study, we show that the selective D1 agonist A77636 also induces orofacial dyskinesia when injected into the subthalamic nucleus of awake rats, thus confirming a role for D1 receptors in this effect. We also examined the dyskinesia induced by intrasubthalamic injections of apomorphine in rats with an ipsilateral lesion of the nigrostriatal pathway. The orofacial response to local administration of apomorphine (1.0 μg) into the subthalamic nucleus was markedly increased in the lesioned rats. As in control rats, the enhanced behavioral response seen in lesioned rats was blocked by peripheral administration of D1 antagonists. Although D1 receptor binding autoradiography revealed no difference in D1 receptor binding in the subthalamic nucleus on the side of the lesion compared to controls, D1 binding was higher in the subthalamic nucleus on the side of the lesion compared to the contralateral side. The increased behavioral response observed after unilateral dopamine denervation suggests that the subthalamic nucleus is tonically regulated by dopaminergic projections from the substantia nigra. Furthermore, the data suggest that subthalamic D1 receptors may be involved in the development of dyskinesia induced by dopaminergic drugs. Synapse 37:298–307, 2000. © 2000 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Grèce</li><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Mehta, Arpesh" sort="Mehta, Arpesh" uniqKey="Mehta A" first="Arpesh" last="Mehta">Arpesh Mehta</name></region><name sortKey="Chesselet, Marie Rancoise" sort="Chesselet, Marie Rancoise" uniqKey="Chesselet M" first="Marie Rançoise" last="Chesselet">Marie Rançoise Chesselet</name></country><country name="Grèce"><noRegion><name sortKey="Thermos, Kyriaki" sort="Thermos, Kyriaki" uniqKey="Thermos K" first="Kyriaki" last="Thermos">Kyriaki Thermos</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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