Eye-blink rates and platelet monoamine oxidase activity in chronic schizophrenic patients.
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Blinking↗
Biomedical subjects
S G Potkin
Publications and source records attributed to S G Potkin.
Dopamine-beta-hydroxylase, monoamine oxidase, and schizophrenia.
Plasma dopamine-beta-hydroxylase (DBH) activity was studied in two different populations of chronic schizophrenic patients and assayed by two independent laboratories. No significant difference between schizophrenic patients and normal controls was found although in both groups chronic undifferentiated schizophrenics with paranoid features had a trend towards lower DBH activity than the other patients and controls. In addition, DBH and monoamine oxidase (MAO) activities were studied in 13 schizophrenic patients and available first degree-relatives. There was no association of low MAO and low DBH activities within the schizophrenic families.
Blood Platelets↗
Phenylethylamine in paranoid chronic schizophrenia.
Phenylethylamine (PEA) is an endogenous amine that is structurally and pharmacologically related to amphetamine. Urinary PEA excretion is significantly higher in paranoid chronic schizophrenics than in nonparanoid chronic schizophrenics and normal controls. Diet, hospitalization, and medication do not account for differences in PEA concentrations. These findings offer some indication that PEA may be an endogenous amphetamine.
Chronic Disease↗
Tardive dyskinesia--reversible and persistent.
Twenty-one hospitalized patients over 50 years of age who had tardive dyskinesia were studied for 13 months. After withdrawal of neuroleptics and antidepressants for three months, dyskinetic symptoms abated in 12 patients and persisted in nine. Discriminant function analysis showed that the persistent and reversible dyskinesia groups could be clearly separated and that the best discriminator was the number of drug-free intervals. The persistent dyskinesia group had had significantly longer neuroleptic treatment (mean, 10.8 yr) and a greater number (mean, 5.6) of drug interruptions of at least two months' duration each than did the reversible dyskinesia group. Our finding, as well as the literature reviewed, does not support the commonly held notion that frequent lengthy interruptions of long-term drug treatment reduce the incidence of persistent dyskinesia, at least in patients who are otherwise predisposed to the development of tardive dyskinesia.
Aged↗
Some kinetic parameters of platelet monoamine oxidase in chronic schizophrenia.
The michaelis constants (Vmax and Km) for platelet monoamine oxidase (MAO) with tyramine as substrate are found to be significantly lower in chronic schizophrenic patients than in normal controls. Furthermore, these kinetic parameters for the MAO of paranoid chronic schizophrenics are significantly lower than those for nonparanoid chronic schizophrenics. Paranoid chronic schizophrenia may be a separate biochemical disorder from other chronic schizophrenias.
Blood Platelets↗
Platelet monoamine oxidase: studies on the rate of heat inactivation in normal and in paranoid and nonparanoid chronic schizophrenic groups.
The heat inactivation curves for platelet monoamine oxidase (MAO) in chronic schizophrenic and normal subjects were virtually identical. There were also no differences found when schizophrenic patients were subgrouped into paranoid and nonparanoid types. However, the MAO from one of the normal subjects showed a substantially greater thermolability than that of any other control or schizophrenic subject.
Blood Platelets↗
Platelet monoamine oxidase activity in schizophrenia: a review of the data.
The authors review studies of platelet and white cell monoamine oxidase (MAO) activity in schizophrenic patients. The data on acute schizophrenic patients remain inconclusive. Review of 26 reports of chronic schizophrenic patients leaves little doubt, however, that there is a subgroup in which the enzyme activity is decreased. Despite the strong association of decreased MAO activity and chronic schizophrenia, the etiological relationship of low platelet MAO activity to schizophrenia has not been demonstrated. More complete diagnostic descriptions will shed light on precisely which patients have lowered MAO activity. Further metabolic investigations with such patients are needed to determine the physiological significance of this phenomenon.
Acute Disease↗
Are paranoid schizophrenics biologically different from other schizophrenics?
Two studies were undertaken to verify the presence of lowered platelet monoamine oxidase activity in chronic schizophrenia. In the first study, a retrospective chart analysis, the mean platelet activity of patients with chronic schizophrenia (7.73+/-0.64 nmol of benzylaldehyde product per 10(8) platelets per hour [S.E.M.]) differed significantly from that of normal controls (12.13+/-0.2, P less than 0.001). Chronic paranoid schizophrenics (4.81+/-0.46) differed significantly from chronic nonparanoid schizophrenics (8.6+/-0.75, P less than 0.03). A separate prospective study confirmed significantly lower values for monoamine oxidase activity in chronic schizophrenic patients diagnosed as paranoid (5.97+/-1.17) or as having secondary paranoid features (6.28+/-0.71) as compared to chronic nonparanoid schizophrenics (9.81+/-0.87, P less than 0.001). Chronic paranoid schizophrenia may be a separate disorder from the other chronic forms of schizophrenia, and this difference may be related, at least in part, to biochemical characteristics.
Blood Platelets↗
Baclofen: lack of effect on human plasma prolactin.
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Aminobutyrates↗
Presence of free, sulfate and glucuronide conjugated 3-methoxy-4-hydroxyphenylglycol (MHPG) in human brain, cerebrospinal fluid and plasma.
The concentration of the free, glucuronide and the sulfate conjugated forms of 3-methoxy-4-hydroxyphenylglycol (MHPG) were measured in human plasma, cerebrospinal fluid (CSF) and brain by mass fragmentography. All three forms of MHPG were detected in the media analyzed. Free MHPG was found to be the predominant form in both the brain and the CSF. The sulfate conjugate of MHPG constitutes about 15% of the total MHPG in the CSF while in the brain the percentage varies between 30% in the hypothalamus and cortex and 80% in the substantia nigra. The concentration of the glucuronide conjugate of MHPG measured in the brain and CSF represents about 5% of the total MHPG concentration. In the plasma free MHPG and its glucuronide and sulfate conjugates are present in about equal concentrations. The relative concentrations of the three forms of MHPG measured in plasma, CSF and brain were compared with their concentrations in the urine from previously published results. From this comparison the diagnostic significance of each of the three forms of MHPG in the clinical assessment of central norepinephrine metabolism is discussed.
Adult↗
Suicide prevention centers. Ecological study of effectiveness.
While suicide prevention services are continually expanding, efforts to measure their efficacy are seldom found in the literature. This study examines the effect of suicide prevention centers in North Carolina on the suicide rate in 1970. The data are examined in a ecological context, i.e., pertinent demographic variables are included in the analysis of the suicide rate in North Carolina counties with an emphasis on structural and contextual effects. A review of the literature on suicide prevention center efficacy, a description of those counties in North Carolina that support such centers, and a rigorous testing of their effect on the countywide suicide rate are undertaken in the present analysis. All of the analyses of the data indicate that the centers have minimal effect on the suicide rate.
Adult↗
Plasma concentrations of some acidic and alcoholic metabolites derived from m- and p-tyramine, octopamine and catecholamines in humans.
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3,4-Dihydroxyphenylacetic Acid↗
Neuropathological studies of brain tissue in schizophrenia.
Postmortem neuropathological investigations in the last half decade provide increasing evidence compatible with a neurodevelopmental defect in schizophrenia. Basic and clinical data support hypotheses suggesting that disturbances in neurodevelopment in schizophrenia may involve the cortical subplate and a theorized second trimester "window of vulnerability". The focus of this paper is on (1) selected methodological issues involved in the collection, analyses and preservation of human postmortem brain tissue; (2) a review of evidence showing morphological defects particularly in prefrontal cortical regions of the schizophrenic brain; and (3) potential future research directions.
Brain↗
GABAA receptor subunit gene expression in human prefrontal cortex: comparison of schizophrenics and controls.
The prefrontal cortex of schizophrenics is hypoactive and displays changes related to inhibitory, GABAergic neurons, and GABAergic synapses. These changes include decreased levels of glutamic acid decarboxylase (GAD), the enzyme for GABA synthesis, upregulation of muscimol binding, and downregulation of benzodiazepine binding to GABAA receptors. Studies in the visual cortex of nonhuman primates have demonstrated that gene expression for GAD and for several GABAA receptor subunit polypeptides is under control of neuronal activity, raising the possibility that similar mechanisms in the hypoactive prefrontal cortex of schizophrenics may explain the abnormalities in GAD and in GABAA receptor regulation. In the present study, which is the first of its type on human cerebral cortex, levels of mRNAs for six GABAA receptor subunits (alpha 1, alpha 2, alpha 5, beta 1, beta 2, gamma 2) and their laminar expression patterns were analyzed in the prefrontal cortex of schizophrenics and matched controls, using in situ hybridization histochemistry and densitometry. Three types of laminar expression pattern were observed: mRNAs for the alpha 1, beta 2, and gamma 2 subunits, which are the predominant receptor subunits expressed in the mature cortex, were expressed at comparatively high levels by cells of all six cortical layers, but most intensely by cells in lower layer III and layer IV. mRNAs for the alpha 2, alpha 5, and beta 1 subunits were expressed at lower levels; alpha 2 and beta 1 were expressed predominantly by cells in layers II, III, and IV; alpha 5 was expressed predominantly in layers IV, V, and VI. There were no significant changes in overall mRNA levels for any of the receptor subunits in the prefrontal cortex of schizophrenics, and the laminar expression pattern of all six receptor subunit mRNAs did not differ between schizophrenics and controls. Because gene expression for GABAA receptor subunits is not consistently altered in the prefrontal cortex of schizophrenics, the previously reported upregulation of muscimol binding sites and downregulation of benzodiazepine binding sites in the prefrontal and adjacent cingulate cortex of schizophrenics are possibly due to posttranscriptional modifications of mRNAs and their translated polypeptides.
Autoradiography↗