Effect of mazindol on brain dopamine turnover in spiperone-treated rats

Fuller, Ray W.; Snoddy, Harold D.

doi:10.1007/bf01252698

Cited by 15 publications

(2 citation statements)

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“…3) confirms our earlier findings (Fuller and Snoddy, 1979). This potentiation has been observed with other dopamine uptake inhibitors besides mazindol, including amfonelic acid, methylphenidate and cocaine (Shore, 1976).…”

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confidence: 88%

Fluoxetine at anorectic doses does not have properties of a dopamine uptake inhibitor

Fuller

Hemrick‐Luecke

Snoddy

1994

J. Neural Transmission

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Although fluoxetine is a highly selective inhibitor of serotonin uptake in vitro and in vivo, some investigators have suggested that dopamine uptake inhibition may contribute to anorectic actions of fluoxetine. The present experiments were done to determine fluoxetine's effects in some animal protocols in which dopamine uptake inhibitors have characteristic actions. Mazindol prevented the depletion of striatal dopamine and its metabolites by amphetamine in iprindole-pretreated rats, but fluoxetine had no effect. Mazindol prevented the depletion of striatal dopamine and its metabolites by 6-hydroxydopamine injected intracerebroventricularly into rats, but fluoxetine had no effect. Mazindol enhanced the elevation of 3,4-dihydroxyphenylacetic acid concentration in rat brain after spiperone injection, but fluoxetine did not cause that effect. Fluoxetine did not mimic amfonelic acid in antagonizing the retention of alpha-methyl-m-tyramine invant striatum after the injection of alpha-methyl-m-tyrosine. These results show that fluoxetine, at doses that are effective in blocking the serotonin uptake carrier and causing anorexia, does not block the dopamine uptake carrier.

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Section: ~/ ~////////////G////////~supporting

confidence: 88%

Fluoxetine at anorectic doses does not have properties of a dopamine uptake inhibitor

Fuller

Hemrick‐Luecke

Snoddy

1994

J. Neural Transmission

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“…This enhanced response is presumably mediated by the combined effects of increased dopamine impulse flow by haloperidol (Bunney et a!., 1973) and blockade of the removal of dopamine by the norepinephrine transporter. This effect is analogous to the synergistic effect of haloperidol and dopamine uptake blockers on dopamine metabolism or release in the striatum (Fuller and Snoddy, 1979;Shore et al, 1979;Westerink et al, 1987;Gudelsky et a!., 1992). It should be acknowledged, however, that evidence is lacking in support of a long-loop negative feedback pathway regulating mesocortical dopamine transmission that would help explain the effect of haloperidol to increase dopamine in the medial prefrontal cortex.…”

Section: Discussionmentioning

confidence: 95%

Regulation of Extracellular Dopamine by the Norepinephrine Transporter

Yamamoto

Novotney

1998

Journal of Neurochemistry

207

143

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There is growing evidence of an interaction between dopamine and norepinephrine. To test the hypothesis that norepinephrine terminals are involved in the uptake and removal of dopamine from the extracellular space, the norepinephrine uptake blocker desmethylimipramine (DM1) was infused locally while the extracellular concentrations of dopamine were simultaneously monitored. DM1 increased the extracellular concentrations of dopamine in the medial prefrontal cortex and nucleus accumbens shell but had no effect in the striatum. The combined systemic administration of haloperidol and the local infusion of DM1 produced an augmented increase in extracellular dopamine in the cortex compared with the increase produced by either drug alone. This synergistic increase in dopamine overflow is likely due to the combination of impulse-mediated dopamine release produced by haloperidol and blockade of the norepinephrine transporter. No such synergistic effects were observed in the nucleus accumbens and striatum. Local perfusion of the a 2-antagonist idazoxan also increased the extracellular concentrations of dopamine in the cortex. Although the stimulation of extracellular dopamine by idazoxan and DM1 could be due to the increased extracellular concentrations of norepinephrine produced by these drugs, an increase in dopamine also was observed in lesioned rats that were depleted of norepinephrine and challenged with haloperidol. This contrasted with the lack of an effect of haloperidol on cortical dopamine in unlesioned controls. These results suggest that norepinephrine terminals regulate extracellular dopamine concentrations in the medial prefrontal cortex and to a lesser extent in the nucleus accumbens shell through the uptake of dopamine by the norepinephrine transporter. Key Words: Norepinephrifle-Dopamine-Cortex--Transporter.

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