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J J Feigenbaum

Publications and source records attributed to J J Feigenbaum.

41 records · Page 3Linked to original sources

Mechanisms of dopamine antagonism by morphine in rodents.

A number of investigators have concluded on the basis of a substantial and compelling body of biochemical, pharmacological and behavioral evidence, that opiates and particularly morphine, directly block central dopamine (DA) receptors. This evidence includes the recent finding that cataleptogenic doses of morphine suppress 3H-spiroperidol binding to striatal membranes ex vivo. On the other hand, an important albeit relatively sparse literature of experimental evidence exists suggesting that morphine and other mu-receptor opiates do not directly bind to central dopaminergic receptors. The most convincing evidence to this effect are behavioral findings that morphine potentiates rather than inhibits the stereotyped behavior induced by the direct DA agonist apomorphine and biochemical evidence demonstrating a failure of 3H-morphine or 3H-dihydromorphine to specifically bind central DA receptors in striatal tissue. (Indeed, even those reports that demonstrated a morphine induced suppression of 3H-spirioperidol labelling of DA receptors failed to find a direct effect on post-synaptic receptors.) Evidence is presented in this report to show that morphine acts presynaptically to acutely inhibit DA release, and thus, that morphine inhibition of DA receptor mediated responses is indirect, being the result of an inhibition of pre-synaptic DA release rather than a direct effect exerted on post-synaptic DA receptors themselves.

Animals↗

The role if dopamine and norepinephrine uptake inhibition in mediating the central effects of d-amphetamine in vivo.

Male Sprague-Dawley rats were injected with 1.5 mg/kg d-amphetamine and later sacrificed at a time when the locomotor activity induced by this dose of d-amphetamine was maximal (60 minutes post injection). Subsequently, both cortical and striatal slices were measured for 3H-DA and 3H-NE uptake. It was found that in vivo, d-amphetamine does not preferentially inhibit the reuptake of DA or NE in either the striatum or cerebral cortex, suggesting that any selective effect on a specific catecholamine must result from a mechanism other than selective uptake inhibition.

Animals↗

Lessened sensitivity to apomorphine induced climbing behavior in mice following neonatal exposure to phenobarbital.

Heterogeneous HS/Ibg mice were injected daily with 50 mg/kg phenobarbital (PhB) from age 2 to 21 days (B group), while control litter mates received vehicle injections. Control and a B mice were then tested for striatal climbing behavior induced by 2 or 5 mg/kg apomorphine, at ages 22, 28, 35 or 44 days. At age 22 days B mice had reductions of climbing from control levels of 44% and 41% for 2 and 5 mg apomorphine respectively (p less than 0.01), regardless of sex differences. On day 28 the respective reductions were 16% and 32% (p less than 0.05). The differences on days 35 and 44 were small and did not reach statistical significance. Since climbing has been found to be induced primarily by postsynaptic striatal dopaminergic receptors, it is suggested that neonatal exposure may reduce the behaviors mediated by striatal postsynaptic dopamine receptors. The present findings support other studies implicating postsynaptic striatal dopamine receptors in the behavioral alterations induced by early PhB exposure.

Animals↗