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Biomedical subjects

V Glover

Publications and source records attributed to V Glover.

192 records · Page 11Linked to original sources

Migraine and depression: biological aspects.

There is a considerable overlap in migraine and depression incidence, and both conditions may be associated with low levels of 5-hydroxytryptamine (5-HT). During a migraine attack there is evidence for low levels of platelet 5-HT and possibly also low Vmax for 5-HT uptake; both these findings are also associated with the depressed state. Both conditions can be treated by tricyclic and monoamine oxidase inhibiting antidepressants. However, there are also clear differences: migraine attacks are brief and self limiting. Part of the migraine cascade occurs outside the blood brain barrier, presumably involving blood vessels and, unlike depression, migraine attacks can be ameliorated by drugs which only act peripherally. In addition, migraine patients, especially males, often have permanently low levels of platelet monoamine oxidase activity, whereas patients with unipolar depression tend to have raised levels of this marker. This low enzyme activity may reflect part of the vulnerability to migraine, often associated in the prodromal phase with agitation or hyperactivity. Migraine may form part of a family of brief recurrent self-limiting disorders, which involve disturbances of both mood and monoamines; during the headache phase of the attack, the links with depression are most apparent.

Blood Platelets↗

Long-term effects of pergolide and (-)-deprenyl on 3H-mazindol and 3H-spiperone binding in rat brain.

The effects of long-term administration of the putative neuroprotective agents pergolide and (-)-deprenyl was assessed by studying 3H-mazindol and 3H-spiperone binding at 12 and 20 months in the major dopamine brain regions. Male Wistar rats were treated from 3 to 20 months, together with their respective untreated and saline injected control groups. The main findings were: 1) there was a decrease in both 3H-mazindol and 3H-spiperone binding with age between 12 and 20 months; 2) there were no differences at 20 months between the pergolide or the (-)-deprenyl treated groups and their controls, thus providing no evidence for long-term neuroprotection; and 3) there was a marked decrease in 3H-mazindol binding in the injected controls compared with the untreated controls at both 12 and 20 months. This raises the possibility that mild chronic stress may accelerate the aging of the dopamine system.

Animals↗

[Effect of isatin on the electrical activity in the rat hippocampus cells].

In vitro superfusion of rat hippocampal slices with isatin changed the population spikes. Isatin perfusion produced two clear effects. 50 microM isatin it increased the amplitude of the population spike in the CA1 evoked by stimulation of stratum radiatum. This effect was readily reversible. 100 microM isatin decreased the population spike amplitude with minimal effect on its latency. High initial response were more suppressed. This effect on the population spike amplitude was not eliminated even after 1 h of washing with saline. The data obtained suggest that isatin-induced electrophysiological changes are involved into the anticonvulsant effect of isatin.

Action Potentials↗

[Interaction of pyruvate kinase with isatin and deprenyl].

The glycolytic enzyme, pyruvate kinase, exhibits moderate affinity [3H]isatin binding (KD approximately 10 microM), which is inhibited by ATP (IC50 25 microM) and deprenyl (IC50 5 microM). Interaction of pyruvate kinase with isatin and its inhibition by ATP and deprenyl has also been confirmed using an independent biosensor technique and immobilized isatin analogue, aminoisatin. This effect has some specificity because the enzyme, creatine phosphokinase, does not exhibit specific isatin-binding. It is suggested that interaction of pyruvate kinase with isatin may reflect some non-glycolytic functions of this enzyme.

Animals↗

[Isatin: possible role in functional interaction of natriuretic peptides and monoamines].

Isatin is an endogenous compound recently discovered in mammalian tissues and body fluids. It has a distinct distribution in rat brain, with a highest concentration, in the hippocampus, of 0.1 microgram/g. Its origin and metabolic pathways remain unclear. In vitro, isatin selectively inhibits monoamine oxidase (MAO) B (IC50 3-8 microM, Ki approximately 20 microM) and, more potently, atrial natriuretic peptide(ANP) binding (IC50, 0.4 microM). Convulsant doses of pentylene tetrazole result in increased isatin level in the brain. Small amounts of isatin are anxiogenic in rodent models, but higher doses cause sedation and possess anticonvulsant action. Isatin administration also increases monoamine levels in the brain and reduces daily urine output.

Animals↗