Effect of acromegaly, hypophysectomy and hypothyroidism on plasma glucose, insulin and free fatty acid responses to a glucose load.
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Acromegaly↗
Biomedical subjects
A Reches
Publications and source records attributed to A Reches.
Neurotensin interacts with dopaminergic neurons in rat brain.
Neurotensin (NT) injected intracerebroventricularly in rat increases dopamine (DA) turnover in the corpus striatum and nucleus accumbens. Significant increases in 3,4-dihydroxyphenylacetic acid (DOPAC) levels occurred within 15 minutes after injection with peak levels at 60 minutes. The effect on NT on DOPAC and homovanillic acid (HVA) accumulation was dose-dependent at 3-100 micrograms. NT, like haloperidol, stimulated 3,4-dihydroxyphenylalanine (DOPA) accumulation in striatal neurons, in the presence of DOPA decarboxylase inhibitor, after injection of gamma-butyrolactone (GBL). NT had a similar stimulatory effect on DOPA levels in the accumbens while haloperidol (0.25 mg.kg-1) had no significant effect in this brain region. NT did not block the inhibitory effect of apomorphine on DOPA accumulation in both the striatum and accumbens, while haloperidol inhibited apomorphine effect in both regions. NT also failed to displace 3H-spiperone from DA receptors and the presence of NT in the binding assay did not alter the ability of DA to displace 3H-spiperone in either brain region. These experiments demonstrate that NT increases DA turnover in both the nigrostriatal and mesolimbic pathways.
3,4-Dihydroxyphenylacetic Acid↗
Superoxide dismutase activity is not affected by closed head injury in rats.
Superoxide anion radicals are generated in association with prostaglandin production, and are implied in the mediation of secondary brain damage following cerebral ischemia or injury. In a model of closed head injury in rats we have demonstrated the activation of phospholipase A2 (PLA2) and the increased production of eicosanoids in the post-trauma period. In the present study we investigated the role of superoxide dismutase (SOD) in this model. Head trauma was induced over the left cerebral hemisphere of ether anesthetized rats by a calibrated weight drop device. Cortical tissue samples were taken 15 min, 4 and 24 h later. SOD activity was assayed by its ability to inhibit the xanthine oxidase-cytochrome c reduction. There was no significant change in SOD activity in any of the regions studied - the site of injury, and contralateral region as well as the remote frontal lobes of both hemispheres. Although intense PLA2 activity and production of eicosanoids was previously found in some of these regions, activity of SOD was unaffected. These results do not support an important role for endogenous SOD up to 24 h after head injury.
Animals↗
Residual neurobehavioral impairment in a water technician exposed to hydrazine-containing mixtures.
Residual neurobehavioral impairment in concentration, comprehension, memory, task performance and mood status persisted in a water technician with respiratory and dermal exposures to hydrazine-containing mixtures prior to treatment with steroids for concurrent thrombocytopenia. The findings call attention to the possibility that residual neurobehavioral impairment may be an effect of exposure to hydrazine mixtures.
Adult↗