Platelet prostaglandin E1 hyposensitivity in schizophrenia: decrease in cyclic AMP formation and in inhibitory effects on aggregation.

Cyclic adenosine monophosphate (cAMP) formation via prostaglandin E1 (PGE1) or forskolin stimulation was determined in washed platelets from 35 schizophrenic patients and 34 normal controls. The inhibitory effects of PGE1 and forskolin on platelet aggregation response (PAR) elicited by adenosine diphosphate (ADP) were also examined simultaneously. Both PGE1- and forskolin-stimulated cAMP formation decreased in platelets from schizophrenic patients, as compared with those from normal controls. PGE1 inhibition of PAR was significantly lowered in schizophrenic patients compared to normal controls, but forskolin inhibition was not. No correlations between PGE1- or forskolin-stimulated cAMP formation and inhibitory effects of PGE1 or forskolin on PAR, respectively, were explained by the complex factors involved in PAR. In conclusion, platelet hyposensitivity to PGE1 in schizophrenic patients is partially based on aberrant adenylate cyclase (AC) activity and includes other variables related to PAR.

Computerised tomography in schizophrenia. Familial versus non-familial forms of illness.

Findings on CT and demographical or clinical data in 80 patients with DSM-III schizophrenia and 45 medical controls were evaluated. Multiple-discriminant analysis showed that the enlargement of the third ventricle and frontal and parietal atrophy could significantly predict the diagnosis of schizophrenia. Widening of Sylvian fissures and parietal atrophy differentiated familial schizophrenics of both horizontal transmission (who had affected siblings) and vertical transmission (who had affected parents or/and offspring) from non-familial patients. Parietal atrophy and a history of birth complications differentiated horizontal from vertical transmission. The CT findings together with some clinical characteristics could differentiate the three subgroups classified by the hereditary form; thus each of these subgroup may belong to a different disease entity, of a different pathophysiology.

Elevated plasma prostaglandin E2 levels in schizophrenia.

Plasma levels of prostaglandin E2 (PGE2) were determined with radioimmunoassay in 40 DSM-III schizophrenics, 15 patients with other mental disorders, and 23 normal controls. The mean value of plasma immunoreactivity of PGE2 was significantly higher in the schizophrenic patients than in the normal controls. Schizophrenic patients with high plasma PGE2 levels had more guilt feelings and hallucinatory behavior on BPRS, relatively successful heterosexual relations, and a higher incidence of birth complications.

Platelet prostaglandin E1 hyposensitivity in schizophrenia: reduction of prostaglandin E1- or forskolin-stimulated cyclic AMP response in platelets.

Cyclic 3',5'-adenosine monophosphate (cAMP) formation via prostaglandin E1 (PGE1)-or forskolin-stimulation were determined in washed intact platelets from 32 schizophrenic patients and 30 normal controls. Regarding basal cAMP levels in the platelets, there were no differences between schizophrenic patients and normal controls. Both PGE1-and forskolin-stimulated cAMP response reduced in platelets from schizophrenics compared with normal controls. These results suggested that platelets in schizophrenics were impaired not only in the adenylate cyclase unit per se but also extensively in the cAMP generating system coupled to a PGE1 receptor.

Substance P involved in mental disorders.

1. This review clarifies the involvement of substance P (SP) in mental disorders, especially schizophrenia. One of the main SP pathways in the brain is the striatonigral pathway. SP applied in the substantia nigra activates the nigro-striatal dopamine system. 2. Administration of antipsychotic drugs decreased SP concentration in the substantia nigra. Some post mortem studies of schizophrenic patients showed elevated SP concentration in some brain regions. Effects of baclofen, a SP antagonist, on schizophrenic patients are uncertain. 3. SP may be involved in the pathophysiology of schizophrenia.