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Effect of piribedil, a D-2 dopaminergic agonist, on dopamine, amino acids, and free radicals in gerbil brain after cerebral ischemia

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Molecular and Chemical Neuropathology

Abstract

The excitatory amino acids (EAA) are involved in the pathogenesis of the cerebral ischemia. Moreover, several investigators have demonstrated that a considerable amount of dopamine (DA) is released in the striatum after ischemia reperfusion/insult (IRI). Recently, studies have demonstrated in vitro, that D-2 agonist, at the level of striatum and retina, may represent a powerful signal to inhibit release of excitatory amino acids implicated in cerebral ischemia. Therefore we have been incited to test, in vivo, the action of a D-2 agonist, piribedil, on gerbil brain after IRI. We have used the Stroke Index (SI); then to precise the mechanism of action, we have determined the levels of dopamine, EAA, and hydroxyl-free radicals (·OH), in striatum, hippocampus, and hemisphere. Piribedil, administered at dose of 10 mg/kg, per os, 60 min before induction of transient cerebral ischemia in gerbils, presents a neuroprotective effect, as measured by SI and significantly reverses the increase of DA, EAA, and ·OH induced by IRI. The mechanism of action of piribedil could be related to its D-2 agonist property.

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Delbarre, B., Delbarre, G., Rochat, C. et al. Effect of piribedil, a D-2 dopaminergic agonist, on dopamine, amino acids, and free radicals in gerbil brain after cerebral ischemia. Molecular and Chemical Neuropathology 26, 43–52 (1995). https://doi.org/10.1007/BF02814940

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  • DOI: https://doi.org/10.1007/BF02814940

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