Added ondansetron for stable schizophrenia: A double blind, placebo controlled trial

Pathophysiological Roles of Serotonergic System in Regulating Extrapyramidal Motor Functions

“…[28][29][30] Recent clinical studies also showed that ondansetron significantly reduced the incidence and severity of antipsychotic-induced EPS (e.g., akathisia and parkinsonism) in patients with chronic schizophrenia. 31,32) In our studies, activation of the serotonergic system by 5-hydroxytryptophan (5-HTP) significantly potentiated haloperidol-induced catalepsy and this 5-HTPpotentiated EPS was also suppressed by systemic treatments or intrastriatal microinjections of ondansetron. 29) These findings indicate that postsynaptic 5-HT 3 receptors in the striatum are involved in the induction or potentiation of extrapyramidal disorders and blockade of the striatal 5-HT 3 receptors can alleviate antipsychotic-induced EPS (Fig.…”

Pharmacological treatment of schizophrenia - a review of progress

“…5-HT3 antagonists such as ondansetron are widely used for the treatment of nausea and are thought to contribute in treating negative symptoms when used together with current antipsychotics. 29 The same studies have also shown reduced incidence of extrapyramidal side-effects. Despite preliminary promising results, a double-blind, placebo controlled clinical trial (NCT00149734) testing the efficacy of ondansetron as adjunct therapy does not have publicly available results.…”

The potential of nicotinic enhancement of cognitive remediation training in schizophrenia

“…Initial research on second-generation antipsychotics generated hope for therapeutic effects to extend into the cognitive domain, but yielded no consistent evidence thereof (Beninger et al, 2010). Other drug classes have been investigated as possible augmentation therapies, such as nicotinic and muscarinic acetylcholine receptor agonists (Martin and Freedman, 2007;Radek et al, 2010;Sellin et al, 2008;Hong et al, 2011), cholinesterase inhibitors Stip et al, 2007), NMDA and AMPA receptor ligands (Goff et al, 2008a(Goff et al, , 2008bLieberman et al, 2009), a D1 agonist (George et al, 2007), a 5-HT3 antagonist (Akhondzadeh et al, 2009), and the analeptic drug Modafinil (Saavedra-Velez et al, 2009). Despite reports of small benefits, no pharmacological add-on strategy has obtained convincing clinical support (Zink et al, 2010).…”