Reversal of neuroleptic-induced orofacial dyskinesia by 5-HT3 receptor antagonists

Naidu, Pattipati S.; Kulkarni, Shrinivas K.

doi:10.1016/s0014-2999(01)00986-4

Cited by 23 publications

(12 citation statements)

References 20 publications

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“…In accord with these findings, it has been shown that 5-HT 3 receptor antagonists ondansetron and tropisetron dose dependently reversed the haloperidol-induced VCMs and reduced haloperidol-induced wet dog shakes, further supporting the possibility of an alteration in the serotonergic system after chronic haloperidol treatment (Naidu and Kulkarni, 2001b). It can be concluded that these 5-HT receptors can serve as potential therapeutic targets for the development of novel molecules for the treatment and prevention of TD.…”

Section: Role Of 5-ht In Apd-induced Extrapyramidal Side Effectssupporting

confidence: 52%

Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

Matteo

Pierucci

Esposito

et al. 2008

Progress in Brain Research

133

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Several recent studies have emphasized a crucial role for the interactions between serotonergic and dopaminergic systems in movement control and the pathophysiology of basal ganglia. These observations are supported by anatomical evidence demonstrating large serotonergic innervation of all the basal ganglia nuclei. In fact, serotonergic terminals have been reported to make synaptic contacts with both substantia nigra dopamine-containing neurons and their terminal areas such as the striatum, the globus pallidus and the subthalamus. These brain areas contain a high concentration of serotonin (5-HT), with the substantia nigra pars reticulata receiving the greatest input. In this chapter, the distribution of different 5-HT receptor subtypes in the basal ganglia nuclei will be described. Furthermore, evidence demonstrating the serotonergic control of basal ganglia activity will be reviewed and the contribution of the different 5-HT receptor subtypes examined. The new avenues that the increasing knowledge of 5-HT in motor control has opened for exploring the pathophysiology and pharmacology of Parkinson's disease and other movement disorders will be discussed. It is clear that these avenues will be fruitful, despite the disappointing results so far obtained by clinical studies with selective 5-HT ligands. Nevertheless, these studies have led to a great increase in the attention given to the neurotransmitters of the basal ganglia and their connections.

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Section: Role Of 5-ht In Apd-induced Extrapyramidal Side Effectssupporting

confidence: 52%

Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

Matteo

Pierucci

Esposito

et al. 2008

Progress in Brain Research

133

View full text Add to dashboard Cite

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“…Spontaneous jaw movements in rats may be influenced by activation of the brain 5-HT system, particularly via 5-HT 1A , 5-HT 2C , and 5-HT 3 receptors 44-46). Acute treatment with the 5-HT 1A agonist, 8-OH-DPAT, reduced haloperidol-induced vacuous chewing movements in rats in a dose-dependent manner, indicating that the serotonergic system is involved in haloperidol-induced dyskinetic movements in the rat model 46)…”

Section: Methodsmentioning

confidence: 99%

Tardive Dyskinesia: Treatment with Aripiprazole

Kang

Kim

2011

Clin Psychopharmacol Neurosci

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Tardive dyskinesia is characterized by choreiform movements, or rhythmic abnormal involuntary movements of the face, mouth, tongue, trunk, and limbs. It is frequently associated with the use of neuroleptic medications. The choreiform movements are irreversible in some patients, even after the drug is withdrawn. Although no reliable treatment for tardive dyskinesia exists, atypical antipsychotics are associated with a significantly lower incidence of tardive dyskinesia than typical antipsychotics. Moreover, recent reports suggest that atypical antipsychotics may have a beneficial effect on tardive dyskinesia remission. Until recently, evidence for the effectiveness of aripiprazole on tardive dyskinesia has been mixed. Aripiprazole has a unique mechanism of action and has various effects in tardive dyskinesia. The drug acts as a partial D2 receptor agonist that can stabilize D2 up-regulation, and as a partial 5-HT1A receptor agonist and a 5-HT2A receptor antagonist, and can increase the release of dopamine in the striatum.

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“…This therapeutic benefit could be related to the ability of 5‐HT 3 receptors to interact with nigrostriatal DA transmission (Sirota et al ., 2000). Behavioural studies indicate that 5‐HT 3 receptors affect motor responses thought to result from an alteration of nigrostriatal DA transmission, such as stereotypy (Shankar et al ., 2000), orofacial dyskinesia (Naidu & Kulkarni, 2001) or rotations (Bachy et al ., 1993). Furthermore, 5‐HT 3 antagonists have been shown to alter the striatal expression of immediate early genes induced by drugs that enhance DA transmission such as amphetamine, cocaine or morphine (Frankel et al ., 1998; Genova & Hyman, 1998; Humblot et al ., 1998).…”

Section: Introductionmentioning

confidence: 99%

Conditional involvement of striatal serotonin₃ receptors in the control of in vivo dopamine outflow in the rat striatum

Porras

Deurwaerdère

Moison

et al. 2003

Eur J of Neuroscience

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Serotonin3 (5-HT3) receptors can affect motor control through an interaction with the nigrostriatal dopamine (DA) neurons, but the neurochemical basis for this interaction remains controversial. In this study, using in vivo microdialysis, we assessed the hypothesis that 5-HT3 receptor-dependent control of striatal DA release is conditioned by the degree of DA and/or 5-HT neuron activity and the means of DA release (impulse-dependent vs. impulse-independent). The different DA-releasing effects of morphine (1 and 10 mg/kg), haloperidol (0.01 mg/kg), amphetamine (1 and 2.5 mg/kg), and cocaine (10 and 20 mg/kg) were studied in the striatum of freely moving rats administered selective 5-HT3 antagonists ondansetron (0.1 mg/kg) or MDL 72222 (0.03 mg/kg). Neither of the 5-HT3 antagonists modified basal DA release by itself. Pretreatment with ondansetron or MDL 72222 reduced the increase in striatal DA release induced by 10 mg/kg morphine but not by 1 mg/kg morphine, haloperidol, amphetamine or cocaine. The effect of 10 mg/kg morphine was also prevented by intrastriatal ondansetron (1 microm) administration. Reverse dialysis with ondansetron also reduced the increase in DA release induced by the combination of haloperidol and the 5-HT reuptake inhibitor citalopram (1 mg/kg). Considering the different DA and 5-HT-releasing properties of the drugs used, our results demonstrate that striatal 5-HT3 receptors control selectively the depolarization-dependent exocytosis of DA only when central DA and 5-HT tones are increased concomitantly.

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Reversal of neuroleptic-induced orofacial dyskinesia by 5-HT3 receptor antagonists

Cited by 23 publications

References 20 publications

Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

Tardive Dyskinesia: Treatment with Aripiprazole

Conditional involvement of striatal serotonin₃ receptors in the control of in vivo dopamine outflow in the rat striatum

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Reversal of neuroleptic-induced orofacial dyskinesia by 5-HT3 receptor antagonists

Cited by 23 publications

References 20 publications

Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

Tardive Dyskinesia: Treatment with Aripiprazole

Conditional involvement of striatal serotonin3 receptors in the control of in vivo dopamine outflow in the rat striatum

Contact Info

Product

Resources

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Conditional involvement of striatal serotonin₃ receptors in the control of in vivo dopamine outflow in the rat striatum