Biomedical subjects

A Di Lauro

Publications and source records attributed to A Di Lauro.

At least 19 recordsLinked to original sources

PubMed1986

Platelet 3H-imipramine binding in bipolar patients.

Platelet 3H-imipramine binding was investigated in 31 control subjects and 19 hospitalized bipolar patients, either in the hypomanic or the depressed phase of illness. The mean Bmax value in the bipolar depressed patients did not differ significantly from that in the control subjects or the hypomanic patients. Differences in timing of the assay after blood collection, membrane preparation, protein content used in the assay, or binding of radioactive ligand to the equipment do not appear to explain the discrepancy between these results and previous findings.

Adult↗

PubMed1986

Glutamate dehydrogenase in human brain: regional distribution and properties.

Glutamate dehydrogenase (GDH) activity was studied in 17 regions of six human brains. Duration and conditions of the postmortem period did not affect enzyme activity. Specific activity ranged between 103 and 377 nmoles/min/mg protein at 25 degrees C and it was 10-fold higher than that found in leukocytes. Apart from exclusively white matter regions (corpus callosum and centrum ovale), there was a moderate regional distribution (2.5-fold variation), with highest values in the inferior olive and hypothalamus, and lowest in the cerebellum and lenticular nucleus. With alpha-ketoglutarate (alpha-KG), NADH, or NH4+ as variable substrate, the apparent Km values in human brain were Km alpha-KG = 1.9 X 10(-3) M, KmNADH = 0.21 X 10(-3) M, and KmNH4+ = 28 X 10(-3) M, and in leukocytes they were Km alpha-KG = 1.7 X 10(-3) M, KmNADH = 0.24 X 10(-3) M, and KmNH4+ = 28 X 10(-3) M. The effects of cofactors, inhibitor, and pH were similar in brain and leukocyte GDH.

Adolescent↗

PubMed1986

No circadian rhythms of serotoninergic, alpha-, beta-adrenergic and imipramine binding sites in rat brain regions.

Bmax values of the specific binding of [3H]-WB 4101, [3H]-dihydroalprenolol, [3H]-spiperone and [3H]-imipramine to various rat brain regions were determined at 4 hr intervals over 24 hr under circadian conditions. No significant circadian rhythm of binding sites number was found for any receptor investigated in cerebral cortex, hypothalamus or brain stem. Some methodological issues are discussed.

Animals↗

PubMed1984

Blood cells as biological trait markers in affective disorders.

Data are reviewed on platelet monoamine oxidase activity, red blood cell/plasma lithium ratio, and tritiated imipramine binding to platelet membranes as trait markers for affective disorders. The results of various studies are not in agreement. Differences in methodological procedure are probably central to such discrepancies. At the present time, no single biological abnormality of blood cells has proved to be a trait marker for affective disorders; thus their use to identify vulnerability to mood disorders or predict favourable response to pharmacological treatment appears to be premature.

Affective Disorders, Psychotic↗

PubMed1982

Specific high-affinity binding of L-[3H]aspartate to rat brain membranes.

The binding of L-[3H]aspartate was investigated in washed membranes prepared from whole rat brain. We were able to differentiate two separate binding sites differing in their Na dependence. The Na-independent binding was saturable, reversible, and optimal at 20 degrees C and at pHs in the neutral range. The dissociation constant (Kd) at 20 degrees C was about 200 nM. This binding site seemed to be modulated by magnesium and calcium at physiological concentrations. None of the amino acids tested was a potent competitor for Na-independent L-[3H]aspartate binding. This binding site was unevenly distributed in the rat central nervous system: cerebellum = cerebral cortex greater than pons-medulla greater than spinal cord. Destruction of the intrinsic neurons of the cerebellum by injecting kainic acid 30 days before sacrifice resulted in a 53% reduction in Na-independent binding in this region. The Na-dependent binding of L-[3H]-aspartate (Kd = 4894 nM) was strongly inhibited by D-aspartate, L-glutamate, D,L-aspartate beta-hydroxamate; was unaffected by calcium and magnesium; and showed a different pattern of distribution: cerebral cortex greater than cerebellum = pons-medulla = spinal cord. This binding in cerebellum was unaffected by injections of kainic acid.

Animals↗

PubMed1981

Is aspartic acid the neurotransmitter of the perforant pathway?

In order to determine whether an amino acid may act as a neurotransmitter in the perforant pathway we examined the effect of lesion of rat entorhinal cortex on the concentrations of various amino acids in the hippocampus proper and fascia dentata. Only the aspartic acid content was found significantly decreased after the lesion. This decreases is not due to a loss from target cells of the perforant pathway, but rather to a loss from its degenerating terminals.

Amino Acids↗

PubMed1980