Biomedical subjects

R Rimon

Publications and source records attributed to R Rimon.

At least 37 records · Page 2Linked to original sources

PubMed1978

Gamma-aminobutyric acid (GABA) in the CSF of schizophrenic patients before and after neuroleptic treatment.

Gamma-aminobutyric acid (GABA) levels in the CSF were measured in 9 normal individuals, 17 drug-free schizophrenic patients and 10 of these same schizophrenic patients after neuroleptic treatment. There was no significant difference between CSF level of GABA in the control group compared to those in schizophrenic patients; however, 6 of the 7 lowest GABA levels were from schizophrenic patients. There was a significant decline of 12 per cent in mean GABA levels in the CSF after a mean of two months of neuroleptic treatment.

Adult↗

PubMed1977

Platelet monoamine oxidase in women with premenstrual syndrome.

Platelet monoamine oxidase (MAO) and RBC catechol-O-methyltransferase (COMT) were studied in 12 women suffering from premenstrual syndrome. No significant variation of platelet MAO or RBC COMT was found during the menstrual cycle, as opposed to previous studies on normal women and monkeys, which report a significant decline of platelet MAO activity in the 5-day period before menses.

Adult↗

PubMed1977

Cyclic AMP in the CSF of patients with schizophrenia.

The dopamine hypothesis of schizophrenia proposes that schizophrenia is associated with increased brain dopaminergic function. Because dopamine is thought to stimulate the production of cyclic AMP in the brain, we hypothesized that CSF cyclic AMP would be increased in schizophrenia. Cyclic AMP in the CSF was determined in 19 schizophrenic patients who had not received neuroleptic treatment in the preceding two weeks. No significant difference could be shown between CSF cyclic AMP in these patients and CSF cyclic AMP in 10 psychiatrically normal controls.

Acute Disease↗

PubMed1976

Cyclic GMP in the CSF of patients with schizophrenia before and after neuroleptic treatment.

Cerebrospinal fluid (CSF) cyclic GMP may derive from central cholinergic neurotransmission. Measurement of CSF cyclic GMP may allow evaluation of possible implications of the dopaminergic hyperactivity in schizophrenia proposed by the dopamine hypothesis. The CSF cyclic GMP levels in 27 drug-free schizophrenic patients was measured and compared to that in 9 psychiatrically-healthy individuals. The mean CSF cyclic GMP level of the schizophrenic patients was 23 per cent lower than that of the control group, but this difference did not attain statistical significance. In addition the CSF cyclic GMP levels in a group of 10 schizophrenic patients were compared before and after 2 months of neuroleptic treatment. The mean level of cyclic GMP rose 50 per cent after treatment with phenothiazines (P less than 0.05). These results could indicate some tendency for decreased activity of central cholinergic neurons in schizophrenia as well as a restored dopaminergic-cholinergic balance after neuroleptic treatment.

Antipsychotic Agents↗

PubMed1976

The effect of haloperidol on epinephrine-stimulated adenylate cyclase in humans.

Administration of epinephrine in man has been shown previously to lead to a rise in plasma cyclic AMP levels by activation of the beta-adrenergic-stimulated adenylate cyclase. Therapeutic doses of lithium in humans block the epinephrine-induced rise in plasma cyclic AMP levels, suggesting that lithium inhibits beta-adrenergic adenylate cyclase. In contrast, ten subjects receiving haloperidol, a druh also effective in the treatment of mania, show a mean rise in plasma cyclic AMP levels after epinephrine administration and the magnitude of the response is the same as for non-drug treated individuals. These findings are discussed in relation to the possible pharmacological mechanisms of action of lithium and haloperidol in the control of mania.

Adenylyl Cyclases↗

PubMed1976

Lithium inhibition of adrenaline-stimulated adenylate cyclase in humans.

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Adenylyl Cyclases↗

PubMed1976

Electrophoresis of platelet monoamine oxidase in schizophrenia and manic-depressive illness.

Monoamine oxidase is an important enzyme in the catabolism of biogenic amines and can be measured in human platelets. Platelet MAO has been reported to be reduced in schizophrenic and manic-depressive patients, though other reports are contradictory. The present study evaluated the possibility that qualitative genetic enzyme abnormalities of MAO could be responsible for the different enzyme activities of platelet MAO in different populations. However, polyacrylamide gel electrophoresis of platelet MAO from 10 manic-depressive, 12 schizophrenic, and 11 normal individuals did not reveal any genetic mutant forms.

Adult↗

PubMed1976

Neuroleptics reduce spinal fluid cyclic AMP in schizophrenic patient.

Cyclic AMP in the cerebrospinal fluid (CSF) was determined in a group of 10 schizophrenic patients before neuroleptic drug treatment and after a mean of 8 week's antipsychotic drug therapy. For 8 patients with marked to moderate treatment response a significant (p less than 0.01) decline in CSF cyclic AMP was observed. This result is consistent with the theory that blockade of postsynaptic dopamine receptors is a major mechanism of the antipsychotic action of neuroleptic drugs.

Acute Disease↗

PubMed1976

Platelet monoamine oxidase in schizophrenia and manic-depressive illness.

Monoamine oxidase (MAO) is an important enzyme in the catabolism of brain biogenic amines. Platelet MAO has been reported to be moderately reduced in manic-depressive patients and markedly reduced in schizophrenic patients. This enzyme's activity has been shown to be under a large degree of genetic control and has been proposed as a 'genetic marker' in schizophrenia. A transcultural replication of the finding of low platelet MAO in schizophrenia and manic-depressive illness was carried out at the Jerusalem Mental Health Centre. Manic-depressive patients were found to have higher platelet MAO activity than schizophrenic patients, as reported previously, but control individuals were as low as the schizophrenic patients. It is unlikely that platelet MAO activity is a transculturally-valid marker for schizophrenia.

Adult↗

PubMed1976

Electrophoretic pattern of red blood cell catechol-o-methyltransferase in schizophrenia and manic-depressive illness.

Human red blood cell (RBC) catechol-O-methyltransferase (COMT) was analyzed by polyacrylamide gel electrophoresis (PAGE). One major enzyme band (B) is observed after electrophoresis. In addition, a minor band (A) of COMT activity comprising no more than 25% of the total activity, is also detectable. The rate of migration during electrophoresis of both bands of RBC COMT was the same in manic depressive, schizophrenic, and normal individuals. These results did not reveal genetic variations in the COMT molecule among these three groups. Furthermore, when total RBC COMT was measured there were no statistically significant differences between schizophrenic, manic-depressive, and control individuals.

Bipolar Disorder↗

PubMed1974