M V Nicholson

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Glucose is the principal energy substrate for the brain and studies have shown that the brain is able to increase glucose availability in the face of glucose starvation (neuroglycopaenia). The mechanisms, believed to be hypothalamic, that may be involved in a brain/blood glucose control system have not yet been identified. We have used novel techniques for(More)
Glucose release from the liver is mediated by hypothalamic norepinephrine (NE) neuronal activity, but glucose itself (or a metabolite of it) exerts negative feedback effects on central NE activity. The aim of the present study was to investigate a possible role for insulin in these central glucose homeostatic mechanisms. Computerized gas chromatography-mass(More)
Shortly after administration of 6-methoxy-1,2,3,4-tetrahydro-beta-carboline (6-MeOTHBC) and yohimbine to normal or hypothyroid rats [the latter exhibiting chronically elevated levels of serotonin (5-HT) neuronal activity in the hypothalamus] there was a highly significant increase in hypothalamic noradrenaline (NA) activity and in ACTH release concomittant(More)
The role of central vs. peripheral actions of clonidine was investigated in the rat following the separate and combined administration of clonidine and 2-deoxy-D-glucose (2-DG). Clonidine or 2-DG alone stimulated serum glucose and corticosterone but hypothalamic noradrenaline neuronal activity and ACTH release were stimulated by 2-DG only. The stimulation(More)
Because central noradrenaline neuronal activity is tonically inhibited by noradrenaline (NA) itself via an action at prejunctional alpha 2-adrenoceptors, it was hypothesised that the blockade of central NA synthesis following acute dopamine-beta -hydroxylase (DBH) inhibition might primarily deplete prejunctional NA levels and result in an increase in(More)
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