Glutamatergic mechanisms have been investigated in postmortem brain samples from schizophrenics and controls. D-[3H]Aspartate binding to glutamate uptake sites was used as a marker for glutamatergic neurones, and [3H]kainate binding for a subclass of postsynaptic glutamate receptors. There were highly significant increases in the binding of both ligands to membranes from orbital frontal cortex on both the left and right sides of schizophrenic brains. The changes are unlikely to be due to antemortem neuroleptic drug treatment, because no similar changes were recorded in other areas. A predicted left-sided reduction in D-[3H]aspartate binding was refuted at 5% probability, but not at 10%. Previously reported high concentrations of dopamine in left amygdala were strongly associated with low concentrations of D-[3H]aspartate binding in left polar temporal cortex in the schizophrenics. The findings are compatible with an overabundant glutamatergic innervation of orbital frontal cortex in schizophrenia. The results also suggest that schizophrenia may involve left-sided abnormalities in the relationship between temporal glutamatergic and dopaminergic projections to amygdala.

No abstract

SUMMARY Changes in blood pressure, pulse rate, and plasma catecholamines, renin activity, cortisol, and calcium were studied in 16 normotensive subjects (eight with a family history of hypertension) for 5 hours following ingestion of alcohol-free and alcohol-loaded beer. Both systolic and diastolic blood pressure rose after alcohol consumption; maximum responses occurred at peak blood alcohol concentrations and were significantly higher than those seen after placebo. Pulse rate was also significantly higher after alcohol ingestion and continued to rise throughout the study. There was no difference in the pressor response to alcohol between the groups with and without a family history of hypertension. No difference was found in plasma norepinephrine or epinephrine levels between alcohol and placebo phases. However, subjects with no family history of hypertension had significantly higher plasma norepinephrine levels (p<0.01) than did those with a family history during both the alcohol and placebo phases, although baseline blood pressures were not significantly different. Plasma epinephrine level was similar in both groups. Plasma renin activity was unchanged throughout, but plasma cortisol fell during both phases. Plasma calcium showed a small but significant fall with alcohol consumption in both groups (p<0.001). These results indicate that in normotensive subjects alcohol ingestion causes a rise in systolic and diastolic blood pressure that is not influenced by a family history of hypertension. This effect does not appear to be sympathetically mediated but may be due to a direct vasoconstrictor effect of alcohol, possibly with an alcohol-induced shift in intracellular calcium. Dr. Potter was supported by a research grant from the British Heart Foundation.Address for reprints: Dr. J.F. Potter, Freeman Road Hospital, Newcastle upon Tyne NE7 7DN, UK.Received July 19, 1985; accepted December 30, 1985. and the duration of the study. We have therefore examined, in normotensive subjects, the acute effects of alcohol and placebo on blood pressure in relation to the possible pressor mechanisms. We examined the changes in blood pressure with the rise and fall in blood alcohol levels to determine whether these changes were due to a direct effect of alcohol or were related to a withdrawal response. Subjects and Methods

Eight normotensive male subjects were infused with angiotensin II or phenylephrine in a single blind fashion. Measurements were made of blood pressure and pulse interval every 3 min, and blood drawn for plasma catecholamines at the beginning and end of the infusion. Phenylephrine produced a rise in blood pressure which was associated with a bradycardia in all subjects. A statistically significant relationship between blood pressure and pulse interval was observed in all subjects. In contrast, angiotensin II infusion produced an equal pressor response, but the change in pulse interval was statistically significantly less than that seen following phenylephrine infusion. In seven of eight subjects no significant relationship was observed between blood pressure and pulse interval. Plasma noradrenaline levels were similar before each pressor infusion and were unchanged during each infusion. These observations are consistent with central inhibition of the baroreceptor heart rate reflex by angiotensin II in man.

No abstract