Serotonin receptor (5HTR2A) gene polymorphism has been reported to be associated with clinical phenotypes in schizophrenia. The current study attempted to investigate a relationship between 5HTR2A 102T/C polymorphism and personality traits as well as clinical symptoms in patients with ICD-10 diagnoses of schizophrenia and affective disorders. 5HTR2A genotyping, clinical and psychological assessment were administered to 375 patients, 104 first-degree healthy relatives of the patients and 157 controls. In the patients an association was observed between the 2/2 5HTR2A genotype and scores on the Hypochondriasis scale (MMPI) (ANOVA, F = 4.56; P = 0.011) and trait anxiety (F = 4.21; P = 0.002). A significant difference between 1/1 and 2/2 genotypes has been also found for Neuroticism scores (EPI) (t = 2.18; P = 0.0031). No significant differences by 5HTR2A genotype were observed in either the control or first-degree relatives' group for all scales studied. Positive, negative and psychopathological symptoms emerged higher in the 2/2 genotype patients compared to other genotype carriers. Therefore, the 2/2 genotype may contribute to produce the phenotype, with specific clinical and pathological features in common, regardless of nosologic heterogeneity of psychoses.

Muscle fibres isolated from adult Schistosoma mansoni contracted in a dose-dependent manner when exposed to elevated K+ with a maximum response obtained with 25 mM K+. These contractions were dependent on extracellular Ca2+ since Co2+ (5 mM) or nicardipine (1 μM) blocked the high K+ contractions. Serotonin (300 nM or higher) was required for maintenance of high K+ contractions. With concentrations of serotonin less than 300 nM the response was dose dependent. 5-Methoxytryptamine or α-methylserotonin at 1 μM as well as 10 μM tryptamine were able to substitute for serotonin, but 1 μM 5-carboxyamidotryptamine was ineffective. The order of potency for antagonists (10 μM) was: methiothepin > metergoline > Ly-278,584 = ketanserin. This pattern of responsiveness does not fit well with any known mammalian serotonin receptor subtype. Since forskolin, an adenylate cyclase activator, is able to mimic the action of serotonin and H89, a protein kinase inhibitor, is able to block the effect of serotonin, the effect of serotonin on contractility of the muscle may be via a cAMP-dependent pathway.