PubMed Health⌕ Search

Biomedical subjects

J Rotrosen

Publications and source records attributed to J Rotrosen.

At least 109 records · Page 6Linked to original sources
PubMed1981

A double-blind comparison of trebenzomine and thioridazine in the treatment of schizophrenia.

Forty inpatient volunteers with diagnoses of schizophrenia were randomly assigned to treatment either with trebenzomine or thioridazine in a double-blind study of clinical antipsychotic efficacy following a 1-week placebo treatment. Psychopathology was rated using the Brief Psychiatric Rating Scale (BPRS) and Clinical Global Impression (CGI). There was a significant difference in therapeutic response to the two drugs in that psychopathology decreased significantly for the thioridazine group, but not for the trebenzomine group. Serum prolactin was elevated during treatment with thioridazine, but not with trebenzomine. Side effects were more frequently reported for the thioridazine group. These results fail to confirm previous reports of clinical antipsychotic efficacy for trebenzomine.

Adolescent↗
PubMed1980

Prostaglandins, platelets, and schizophrenia.

Prostaglandin (PG) E1 enhances formation of 3H-adenosine-3',5'-cyclic monophasphate (3H-cAMP) in platelets pulse-labeled with 3H-adenine. This response was assessed as an index of receptor sensitivity and of PG function. Prostagladin E1-stimulated 3H-cAMP accumulation in paltelets from schizophrenics was significantly reduced compared with control subjects. Platelet incorporation of 3H-adenine and basal 3H-cAMP accumulation. We discuss the results in terms of the possible role of PGs in the etiopathology of schizophrenia and derivative implications for treatment.

Adult↗
PubMed1980

Responses to apomorphine, amphetamine, and neuroleptics in schizophrenic subjects.

Twenty-one schizophrenic subjects, who had been neuroleptic-free, were tested for responsiveness to dopaminergic agonists: Apomorphine emesis threshold was determined and change in psychopathology after 0.5 mg/kg d-amphetamine orally was rated. The subjects' subsequent response to neuroleptic treatment were also determined. Sensitivity to apomorphine emesis was also determined in a nonschizophrenic control group. Apomorphine emesis threshold was not significantly different in the schizophrenic and control groups. Correlations were done between baseline psychopathology, apomorphine sensitivity, and changes in psychopathology after amphetamine and after neuroleptic treatment. On the Brief Psychiatric Rating Scale (BPRS), baseline psychopathology correlated with improvement after neuroleptics and, on the clinical global impressions (CGI), increase of psychopathology after amphetamine also correlated with improvement after neuroleptic treatment. An inverse correlation was found between several indices of sensitivity to amphetamine (psychopathology change) and emetic sensitivity to apomorphine. An examination of individual subjects' responses to amphetamine and, subsequently, neuroleptics, suggested that in the absence of significant clinical change after amphetamine a brisk therapeutic response to neuroleptics was rare.

Adult↗
PubMed1980

Metoclopramide: antipsychotic efficacy of a drug lacking potency in receptor models.

Metoclopramide is a substituted benzamide derivative, structurally similar to procainamide and sulpiride. In behavioral, biochemical, and neuroendocrine tests it displays classic neuroleptic dopamine (DA) antagonist properties; in contrast to other DA antagonists, it lacks potency in currently used DA receptor models. In clinical studies using low doses or dubious measures, it was considered not to be efficacious as an antipsychotic. We now find that it indeed has a clinical profile similar to known neuroleptics when used in a dose range predicted from animal models. The findings raise questions regarding the validity and universality of several predictive models, as well as hypotheses purporting to explain molecular mechanisms of action of neuroleptic agents. The drug's inactivity in receptor models suggests that an as yet unidentified DA receptor subpopulation may be important as the mediator of many DA dependent neurobiologic phenomena.

Antipsychotic Agents↗
PubMed1980

Differential effects of amphetamine and neuroleptics on negative vs. positive symptoms in schizophrenia.

Positive symptoms of schizophrenia were diminished by neuroleptics and increased by amphetamine and accounted for most of the change seen in the total Brief Psychiatric Rating Scale (BPRS). Negative symptoms in the same subjects were not affected by neuroleptics but increased after amphetamines to a degree that just attained statistical significance. This increase was due to one item (emotional withdrawal) of the negative symptom factor which responded to neuroleptics and amphetamines as did positive symptoms. These findings are discussed with respect to new ideas about the role of dopamine in schizophrenia.

Adult↗
PubMed1980

Experimental dystonia induced by quaternary-chlorpromazine.

When quaternary-chlorpromazine (Q-CPZ) was administered intraventricularly (ICV) to rats, it induced a lateralized dystonic reaction, which progressed to head-to-tail barrel rolling. The syndrome persisted for approximately 10 minutes, was not antagonized by pretreatment with drugs used to treat extrapyramidal movement disorders, and could not be mimicked by ICV administration of dopamine antagonists. Unlike known dopamine antagonists, Q-CPZ does not alter dopamine turnover, cause prolactin release in vivo, or bind to dopamine/neuroleptic receptors in vitro. These data suggest that Q-CPZ differs substantially from CPZ in pharmacologic action, and that it elicits a behavioral syndrome of potential use for studying dystonias.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Atypical antidopaminergic properties of CI-686: a potential antipsychotic agent.

The effects of the antipsychotic/antidepressant drug CI-686 on apomorphine- and amphetamine-induced stereotypies, dopamine metabolism, neuroleptic binding, and serum prolactin levels were determined. CI-686 displayed profiles of activity in each of these systems that differs markedly from those of other antipsychotics. CI-686's unique preclinical profile suggests a mechanism of action other than dopamine antagonism which could have implications regarding current thinking on the pathophysiology of schizophrenia.

Amphetamine↗
PubMed1979

Behavioral and neuroendocrine effects of low dose ET-495: antagonism by haloperidol.

Low doses of the dopamine agonist ET-495 were administered to nonpsychotic volunteer subjects by slow intravenous infusion, followed by a bolus of 1.5--2.5 mg haloperidol. ET-495 caused progressive dysphoria and sedation (in some cases, light sleep), effects believed to be mediated by dopaminergic inhibition. However, ET-495 also elevated growth hormone and suppressed prolactin, typical responses to dopamine agonist activity. Haloperidol reversed both the sedation and prolactin suppression induced by ET-495. These findings suggest: (1) that the sedation and hormonal responses were produced by stimulation of dopamine receptors; (2) that neurotransmitter systems mediating behavioral and neuroendocrine regulation may have differential neuropharmacological characteristics.

Adult↗
PubMed1979

Neuroendocrine effects of apomorphine: characterization of response patterns and application to schizophrenia research.

Apomorphine, a direct-acting dopamine agonist, stimulates release of growth hormone (hGH) and suppresses release of prolactin (PRL) from the anterior pituitary. Previous studies comparing the magnitude of these responses in schizophrenics and controls suggest that many acute (and some chronic) schizophrenics have exaggerated hGH responses; many chronic schizophrenics (and patients with tardive dyskinesia) have blunted hGH responses to apomorphine, and possibly blunted PRL responses. The present studies extend and confirm these findings in chronic schizophrenics; in addition, several studies were undertaken to further characterize these apomorphine-induced endocrine responses. Studies in which apomorphine was given on 2 or 3 separate occasions to each of five subjects indicate that the hGH response is a highly reproducible individual index, but PRL suppression is a less satisfactory measure. hGH responses to apomorphine were consistently antagonized by pretreatment with haloperidol, supporting the concept that the hGH-releasing effect of apomorphine is mediated by its action on dopamine receptors. Cyproheptadine pretreatment was associated with erratic increases or decreases in the hGH response to apomorphine, but did not alter PRL levels or apomorphine-induced PRL suppression. The relationship of these findings to biological hypotheses of schizophrenia and to neuroleptic-induced receptor changes is discussed.

Adult↗