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Biomedical subjects

K E Moore

Publications and source records attributed to K E Moore.

At least 253 records · Page 14Linked to original sources
PubMed1975

D-amphetamine-induced release of "newly synthesized" and "stored" dopamine from the caudate nucleus in vivo.

The lateral and third ventricles of anesthetized cats were perfused continuously with artificial cerebrospinal fluid (CSF) containing 3H-tyrosine and the perfusate was analyzed for 3H-catecholamines. The addition of d-amphetamine sulfate to the perfusing CSF for 2 hours, beginning 2 hours after the start of the 3H-tyrosine perfusion, caused an immediate increase in the efflux of 3H-dopamine. The efflux of this amine declined subsequently despite the continued presence of amphetamine in the CSF. The addition of alpha-methyltyrosine to the CSF concurrently with the d-amphetamine did not markedly alter the immediate increase but accelerated the subsequent decline in the efflux of 3H-dopamine. This suggests that ampetamine initially releases dopamine from a "strong pool," but continuous release is dependent upon ongoing amine synthesis. The addition of d-amphetamine to the 3H-tyrosine containing CSF at the start of perfusion immediately increased the efflux of 3H-dopamine. This response was completely blocked by the presence of alpha-methyltyrosine in the CSF. Pretreatment of cats with reserpine effectively depleted the caudate nucleus of endogenous and 3H-dopamine, but did not alter the ability of d-amphetamine to increase the efflux of 3H-dopamine. Indeed, the amount of 3H-dopamine released during each collection period by either intraventricular or intravenous administration of d-amphetamine was higher than the content of the labeled amine remaining in the whole caudate nucleus. These results suggest that damphetamine can release both "stored" and "newly synthesized" 3H-dopamine from the caudate nucleus, but that the maintenance of the amphetamine-induced release of dopamine is dependent upon the newly synthetized pool.

Animals↗
PubMed1975

Blockade by reserpine of methylphenidate-induced release of brain dopamine.

The cerebroventricular systems of cats were perfused by introducing artificial cerebrospinal fluid into a lateral ventricle and collecting the perfusate at the aqueduct. 3-H-tyrosine was continuously added to the perfusing cerebrospinal fluid and the perfusate was analyzed for 3-H-catecholamines. Intraventricular or intravenous administration of methylphenidate increased the efflux of 3-H-dopamine. In cats pretreated with reserpine, this response to methylphenidate was reduced while the efflux of 3-H-dopamine caused by delta-amphetamine was slightly increased. These results provide direct biochemical evidence in support of the hypothesis that the central stimulant action of amphetamine and methylphenidate result from their abilities to preferentially release dopamine from "newly synthesized" and "stored" pools, respectively.

Animals↗
PubMed1975

Supersensitivity to dopamine agonists following unilateral, 6-hydroxydopamine-induced striatal lesions in mice.

Following an injection of 6-hydroxydopamine into the left striatum, mice initially circled spontaneously in the direction of the lesion and gradually developed an ability to circle in the opposite direction when challenged with apomorphine or L-dopa. Dose-response curves for apomorphine- and L-dopa-induced circling rates shifted to the left as the duration between the time of the 6-hydroxydopamine injection and the time of testing increased from 2 to 30 days. There was a positive correlation between the rate of apomorphine-induced circling and the reduction in the dopamine concentration in the lesioned forebrain. Doses of apomorphine and L-dopa required to elicit circling responses were 1/6 to 1/10 of those required to increase locomotor activity in normal mice. These data support the concept of development of supersensitivity of postsynaptic dopaminergic receptors in the lesioned striatum.

Animals↗