2001
DOI: 10.1016/s0091-3057(00)00476-7
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Increased m-CPP-induced oral dyskinesia after lesion of serotonergic neurons

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Cited by 18 publications
(10 citation statements)
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“…Conversely, 5-HT 1B , 5-HT 2A or 5-HT 3 antagonists did not modify m -CPP-induced abnormal oral movements while 5-HT 1A , 5-HT 1B or 5-HT 3 agonists did not elicit oral dyskinesia [20, 30, 35]. Oral movements observed after systemic injection of m -CPP were not modified or transiently increased by 5,7-dihydroxytryptamine lesions of 5-HT neurons [36], thus ruling out the action of m -CPP on the 5-HT transporter in this behavioral response. Although these latter data do not exclude a role for 5-HT receptors other than 5-HT 2C ones in the control of orofacial activity, these results emphasize a strong link between oral motor control and 5-HT 2C receptors.…”
Section: Introductionmentioning
confidence: 99%
“…Conversely, 5-HT 1B , 5-HT 2A or 5-HT 3 antagonists did not modify m -CPP-induced abnormal oral movements while 5-HT 1A , 5-HT 1B or 5-HT 3 agonists did not elicit oral dyskinesia [20, 30, 35]. Oral movements observed after systemic injection of m -CPP were not modified or transiently increased by 5,7-dihydroxytryptamine lesions of 5-HT neurons [36], thus ruling out the action of m -CPP on the 5-HT transporter in this behavioral response. Although these latter data do not exclude a role for 5-HT receptors other than 5-HT 2C ones in the control of orofacial activity, these results emphasize a strong link between oral motor control and 5-HT 2C receptors.…”
Section: Introductionmentioning
confidence: 99%
“…Oral dyskinesia observed after peripheral injections of mCPP was enhanced by 5,7-DHTinduced lesion of the serotonergic neurons, probably due to an altered sensitivity to 5-HT 2C receptor stimulation in the STN (Mehta et al, 2001). Interestingly, these authors observed mCPP-induced seizure-like behaviours in a subset of lesioned rats that were never observed in shamlesioned animals, thus demonstrating a pivotal role for the 5-HT 2C receptor in the control of the normal neuronal excitability, a phenomenon already noted by others (Mehta et al, 2001). Despite the fact that the mechanism by which serotonergic inputs to the STN contribute to its normal functioning remains controversial, the behavioural data discussed above clearly suggest that excess stimulation of 5-HT 2C receptors in this region may lead to hyperkinetic movement disorders.…”
Section: -Ht Modulation Of Stn Activitymentioning
confidence: 92%
“…The contribution of the 5-HT 2C receptor in 5-HT-induced behaviour was revealed by the intrasubthalamic injection of the 5-HT 2C receptor agonist MK 212 that, in concordance, increased the net turns (Belforte and Pazo, 2004). In addition, the blockade of subthalamic 5-HT 2C receptors suppressed the stereotypic behaviour induced by apomorphine administration (Barwick et al, 2000) while both systemic administration and local unilateral infusion of mCPP into the STN induced an increase in oral movements in rats (Eberle-Wang et al, 1996;De Deurwaerdere and Chesselet, 2000;Mehta et al, 2001) that resemble the orofacial dyskinesias occurring as a severe side effect of prolonged treatment with antipsychotic drugs in humans (Waddington et al, 1986;Ellison, 1991). Oral dyskinesia observed after peripheral injections of mCPP was enhanced by 5,7-DHTinduced lesion of the serotonergic neurons, probably due to an altered sensitivity to 5-HT 2C receptor stimulation in the STN (Mehta et al, 2001).…”
Section: -Ht Modulation Of Stn Activitymentioning
confidence: 97%
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“…Findings from animal research studies have shown that 5-hydroxytryptamine (5-HT) plays an important role in inducing abnormal oro-facial movements (Eberle-Wang et al, 1996;Mehta et al, 2001). Furthermore, there are multiple clinical reports on the SSRIinduced movement disorders that comprise akathisia, dystonia, dyskinesia, parkinsonism, tardive dyskinesia and mixed disorders (Gerber and Lynd, 1998;Leo, 1996).…”
mentioning
confidence: 99%