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K E Moore

Publications and source records attributed to K E Moore.

At least 235 records · Page 13Linked to original sources
PubMed1977

Increase in dopamine content of the rat median eminence after long-term ovariectomy and its reversal by estrogen replacement.

The norepinephrine (NE) and dopamine (DA) concentrations of the median eminence and the remaining hypothalamus of female rats were assayed using a sensitive radioenzymatic method. There were no changes in the catecholamine concentrations of either brain region when measured in the mornings of the different days of the estrous cycle. Four to 5 weeks after ovariectomy there was a marked increase in the DA but not the NE content of the median eminence, and the daily administration of estradiol benzoate for 7 days prior to sacrifice reversed the ovariectomy-induced increase in DA. Ovariectomy did not alter catecholamine concentrations in the remaining hypothalamus.

Animals↗
PubMed1977

The actions of amphetamine on neurotransmitters: a brief review.

The central stimulant actions of d-amphetamine are not altered in animals in which brain stores of catecholamines have been depleted with reserpine, but they are blocked by alpha-methyltyrosine, which inhibits catecholamine synthesis. The results of a variety of experiments suggest that the central actions of amphetamine result primarily from the ability of the drug to facilitate the release of newly synthesized dopamine from nerve terminals in the forebrain. The results of experiments in animals in which dopaminergic nerve terminals in various brain regions have been selectively destroyed by intracranial microinjection of 6-hydroxydopamine reveal that the locomotor stimulant actions of relatively low doses of amphetamine are dependent upon mesolimbic dopaminergic neurons, whereas the stereotyped behaviors induced by relatively larger doses of amphetamine are dependent upon nigrostriatal dopaminergic neurons. The central actions of amphetamine appear to be the primary result of interactions with dopamine neurons, but secondarily the drug also alters the dynamics of other putative neurotransmitters (e.g. acetylcholine, 5-hydroxytryptamine) in the brain.

Amphetamine↗
PubMed1977

A comparison of the effects of haloperidol on dopamine turnover in the striatum, olfactory tubercule and median eminence.

A sensitive radioenzymatic procedure was used to quantify the effect of haloperidol on dopamine concentrations and rates of turnover in rat striatum, olfactory tubercle and median eminence, regions containing terminals of nigrostriatal, mesolimbic and tuberoinfundibular neurons, respectively. Haloperidol (2.5 mg/kg s.c.) did not alter the steady-state concentrations of dopamine in any of these brain regions at any time. Haloperidol increased dopamine turnover in the striatum and olfactory tubercle 2 and 8 hours after adminstration. The rate of dopamine turnover was increased only in the median eminence 16 and 24 hours after the administration of haloperidol, and effect which was blocked by hypophysectomy. Two other antipsychotic agents, clozapine and thioridazine, also increased dopamine turnover in the median eminence 16 hours after the first of two injections. These results provide evidence for the existence of hormonal neuronal feedback modulation of tuberoinfundibular dopaminergic neurons in contrast to the neuronal feedback modulation of nigrostriatal and mesolimbic neurons.

Animals↗
PubMed1977

Possible significance of clozapine-induced increase in brain dopamine.

Clozapine elevates the concentration of dopamine in the brains of mice injected with doses of 5-20 mg/kg while a 40 mg/kg dose has no effect. This biphasic change in dopamine content is seen in both the striatum and olfactory tubercle. The elevated dopamine concentration is dose-dependently antagonized by apomorphine, while a corresponding clozapine-induced reduction in norepinephrine concentrations is unaffected by apomorphine. These results suggest that part of the action of clozapine may be to reduce the release of dopamine.

Animals↗
PubMed1976

Differential actions of dopamine agonists and antagonists on the gamma-butyrolactone-induced in mouse brain dopamine.

gamma-Butyrolactone (GBL) increased the dopamine concentration in the forebrain of the mouse. Apomorphine dose-dependently antagonized the GBL effect, while piribedil was less effective. Haloperidol prevented the antagonism of GBL by apomorphine but pimozide was ineffective in blocking apomorphine. After chronic treatment with haloperidol or pimozide, there was no alteration of the maximum GBL-induced increase in dopamine nor was there any significant change in the antagonism by apomorphine, although a trend toward increased sensitivity to apomorphine was noted in the group withdrawn from haloperidol. These results suggest that in the mouse, haloperidol is a more effective antagonist of presynaptic dopamine autoreceptors than pimozide, while apomorphine is a better presynaptic agonist than piribedil.

4-Butyrolactone↗
PubMed1976

Differential effects of dopamine agonists and haloperidol on release of prolactin, thyroid stimulating hormone, growth hormone and luteinizing hormone in rats.

The dose-response effects of apomorphine and ET-495 (piribedil), 2 specific dopamine (DA) receptor stimulators, and haloperidol, a DA receptor blocker, were tested on the secretion of prolactin (PRL), thyroid stimulating hormone (TSH), growth hormone (GH) and luteinizing hormone (LH) in male rats. Both apomorphine and piribedil reduced serum PRL and TSH levels, stimulated GH release at low but not at high doses and either had no effect or tended to reduce serum LH levels. The minimal effective dose of apomorphine for reducing PRL by 30 min was 0.01 mg/kg; TSH inhibition was observed with a dose of 0.1-0.3 mg/kg. The inhibitory effects of apomorphine (1.0 mg/kg) on PRL and TSH levels were maximal by 15 min and diminished by 120 min; plasma GH was highest 120 min after injection. Thyroidectomy (10 days) markedLH elevated serum TSH, had no effect on serum PRL and inhibited the ability of apomorphine (0.1 or 0.3 mg/kg) to reduce TSH but not PRL levels. These observations may indicate that separate dopaminergic control mechanisms exist for TSH and PRL secretion. Administration of haloperidol elevated serum PRL, tended to lower TSH, dramatically reduced GH and had no effect on LH levels. Haloperidol pre-treatment blocked the effects of apomorphine on PRL, TSH, and GH secretion. The overall results of this study indicate that DA agonists inhibit PRL and TSH, stimulate GH but do not stimulate LH release in male rats.

Animals↗
PubMed1976

Selective actions of prolactin on catecholamine turnover in the hypothalamus and on serum LH and FSH.

The effects of prolactin (PRL) administration on catecholamine turnover in various brain regions of ovariectomized rats were determined by observing the decline of dopamine and norepinephrine concentrations after alpha-methyltyrosine (alphaMT) administration. PRL had no effect on the steady state concentration of dopamine in the median eminence, anterior hypothalamus and corpus striatum or on the norepinephrine concentration in the anterior hypothalamus. However, PRL selectively enhanced dopamine turnover in the median eminence and anterior hypothalamus after a latent period of 10-26 h. In addition, PRL administration significantly decreased serum concentrations of LH and FSH. These results suggest that the PRL-induced increase in activity of dopaminergic neurons in the median eminence or anterior hypothalamus may be responsible for the reduction of the post-castration rise in serum concentrations of LH and FSH.

Animals↗
PubMed1975

Supersensitivity to dopaminergic agonists induced by haloperidol.

Haloperidol caused a significant reduction in the spontaneous locomotor activity of mice when added to their diet for 11 days. Upon removal of the drug from their diet these mice exhibited withdrawal hyperactivity for several days that was characterized by an increase in activity over control or pre-halopericol values. Similar results were obtained when mice were fed a diet containing pimozide. Withdrawal hyperactivity was not detected after 1 or 3 days of haloperidol containing diet, but was maximal after 6 days of this diet. Dose-response curves of apomorphine-stimulated motor activity and rearing behavior were shifted to the left when determined in mice during the period of withdrawal hyperactivity. Dopaminergic agonists (apomorphine, piribedil, L-DOPA and d-amphetamine) induced gnawing at lower doses in mice removed from a chronic haloperidol-containing diet for 2 days than in mice maintained on a control diet. These results support the hypothesis that prolonged blockade of central dopaminergic receptors by neuroleptics causes subsequent behavioral effects that may be due to the development of enhanced receptor sensitivity.

Animals↗