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Biomedical subjects

K E Moore

Publications and source records attributed to K E Moore.

At least 217 records · Page 12Linked to original sources
PubMed1978

Localization of the site of the haloperidol-induced, prolactin-mediated increase of dopamine turnover in the median eminence: studies in rats with complete hypothalamic deafferentations.

Complete hypothalamic deafferentations were made in male rats with a modified Halász knife to isolate tuberoinfundibular dopaminergic neurons from the rest of the brain. A radioenzymatic procedure was employed to quantify dopamine and norepinephrine concentrations in various regions of the hypothalamus. Dopamine concentrations were unaltered while norepinephrine concentrations were reduced 50% in the median eminence and hypothalamic island 16-33 days after surgery. Basal serum prolactin concentrations were unaltered in these rats but were elevated 16 hours after the injection of haloperidol and 1 hour after alpha-methyltyrosine. The isolation of tuberoinfundibular neurons from the rest of the brain did not alter the ability of haloperidol to increase the rate of alpha-methyltyrosine-induced decline of dopamine in the median eminence. These results indicate that the haloperidol-induced, prolactin-mediated increase of dopamine turnover in the median eminence results from a direct action of this hormone on neurons within the medial basal hypothalamus.

Animals↗
PubMed1978

Regional brain atrophy and reductions in glutamate release and uptake after intrastriatal kainic acid.

1 Neurochemical changes and tissue weights were measured following intrastriatal injection of 2.5 microgram of kainic acid in 2 microliter of 0.9% w/v NaCl solution (saline) in the rat. 2 After kainic acid the striatum and neocortex on the injected side showed a progressive reduction in weight, the neocortex showing the greatest absolute weight loss and the striatum the greatest percentage change. 3 Large (80-90%) reduction in choline acetyltransferase (CAT) and L-glutamate decarboxylase (GAD) activities in the striatum occurred within 2-4 days of the injection and persisted at least 10 weeks. At 10 weeks CAT and GAD activities were unaltered in the neocortex. 4 The absolute content of dopamine in the striatum was not different from control 5 days after the injection of kainic acid but was reduced at 2 and 10 weeks. At 2 weeks the concentration (microgram/g wet weight) of dopamine also was reduced but at 10 weeks it was near normal due to atrophy of the striatum. 5 The high affinity glutamate uptake into a crude synaptosomal preparation of the striatum was reduced by 64% 5 days after kainic acid and still reduced by 67% at 10 weeks. 6 The efflux of glutamate from slices of the striatum in the presence of 52 mM K+ was reduced by approximately 75% 5 days and 15 weeks after kainic acid. 7 In vitro kainic acid (10(-4) M) neither altered the high affinity uptake of radiolabelled glutamate into a homogenate of the striatum, nor released endogenous glutamate from slices of striatum.

Animals↗
PubMed1978

Studies on tuberoinfundibular dopamine neurons.

All dopaminergic neurons in the central nervous system do not respond to pharmacological and endocrinological manipulations in the same manner. Tuberoinfundibular neurons appear to be regulated, in part, by circulating levels of prolactin. Prolactin increases the activity of these neurons by acting directly within the medial basal hypothalamus, possibly on the tuberoinfundibular neurons.

Animals↗
PubMed1978

Tolerance to the effects of baclofen and gamma-butyrolactone on locomotor activity and dopaminergic neurons in the mouse.

Acute injections of baclofen or gamma-butyrolactone (GBL) into mice caused dose-dependent depression of locomotor activity and an elevation of the dopamine content and a reduction of dopamine turnover in the brain. An acute injection of baclofen, but not of GBL, was less effective in producing these effects in mice maintained on a diet containing baclofen for 10 to 12 days. This suggests that baclofen and GBL may influence dopamine neurons by different mechanisms. Acute injections of both baclofen and GBL were less effective in producing behavioral and neurochemical effects in mice pre-treated for 13 days with injections of GBL. Tolerance to the behavioral and neurochemical actions of baclofen and GBL do not appear to be the result of metabolic tolerance but possibly result from changes in the properties of the dopamine neurons.

4-Butyrolactone↗
PubMed1977

Mesolimbic dopamine neurons: effects of 6-hydroxydopamine-induced destruction and receptor blockade on drug-induced rotation of rats.

Bilateral injections of 6-hydroxydopamine (6-OHDA) into the nucleus accumbens greatly reduced the dopamine content of this nucleus and the olfactory tubercle and blocked the ipsilateral rotation induced by amphetamine and methamphetamine in rats with unilateral 6-OHDA lesions of the caudate nucleus. In contrast, apomorphine-induced contralateral rotation was enhanced. Similar results were obtained when the destruction of forebrain noradrenergic neurons, normally produced by the nucleus accumbens 6-OHDA lesion, was prevented by desipramine (DMI) pretreatment. Microinjections of the dopamine receptor antagonist heloperidol into the nucleus accumbens did not spread to the olfactory tubercle, as assessed by the distribution of 3H-haloperidol, and blocked circling induced by amphetamine and apomorphine. Amphetamine-induced circling was less effectively blocked by haloperidol injected into the olfactory tubercle. These results suggest that activity at nucleus accumbens dopamine receptors can greatly affect circling behavior, perhaps by amplifying asymmetries of nigrostriatal activity.

Amphetamine↗
PubMed1977

Increase in mouse brain dopamine content by baclofen: effects of apomorphine and neuroleptics.

Baclofen, like gamma-butyrolactone, causes a dose-dependent increase in the concentration of dopamine in the mouse brain without affecting the content of norepinephrine. This increase is antagonized by apomorphine. Haloperidol but not pimozide counteracts this effect of apomorphine and dose-dependently enhances the increase in brain dopamine produced by baclofen. The results suggest that baclofen reduces impulse flow in dopaminergic neurons in a manner similar to that produced by gamma-butyrolactone.

Aminobutyrates↗
PubMed1977

Effects of estrogen on prolactin and tuberoinfundibular dopaminergic neurons.

Serum prolactin concentrations and dopamine turnover in the striatum and median eminence were studied in male rats after the administration of estradiol benzoate. The alpha-methyltyrosine-induced reduction of dopamine concentrations in these brain regions was used to evaluate relative rates of turnover. Steady state dopamine concentrations in the median eminence and striatum were not altered by 1, 3 or 5 days of estradiol treatment. However, 3 or 5 days of estradiol administration enhanced dopamine turnover in the median eminence but not in the striatum. Estradiol treatment failed to alter dopamine turnover in the median eminence of hypophysectomized rats. Estradiol increased serum prolactin concentrations at all of the times examined. Although alpha-methyltyrosine also increased serum prolactin, this increase was further enhanced in estradiol-treated rats. The increased prolactin response to alpha-methyltyrosine and increased dopamine turnover in the median eminence of estradiol-treated rats suggests that tuberoinfundibular dopaminergic neurons may be part of a hormonal-neuronal negative feedback loop which functions to regulate prolactin secretion.

Animals↗