Effect of pentobarbital on NMDA-evoked release of dopamine in the striatum of awake freely moving rats

• Published in: Japanese Journal of Pharmacology 1996, Vol.71 (suppl.1), p.189-189
• Main Authors: Sugahara, Megumi, Shibanoki, Shinji, Kogure, Miki, Hata, Hideyo, Ishikawa, Koichi
• Format: Article
• Language: eng ; jpn
• ISSN: 0021-5198
• DOI: 10.1016/S0021-5198(19)36995-1

In vivo brain microdialysis was applied to investigate the effects of intravenous anesthetics (pentobarbital, urethane and chloral hydrate) on N-methyl-D-aspartate (NMDA)-evoked dopamine release in the striatum of awake freely moving rats. Pentobarbital (50 mg/kg, i.p.) significantly inhibited the increase of extracellular dopamine concentration by continuous application of NMDA (1 mM) via the probe. However, the effect of NMDA on dopamine was not inhibited by other intravenous anesthetics such as urethane (400 mg/kg, i.p.) and chloral hydrate (400 mg/kg, i.p.). The inhibitory effect of pentobarbital on the NMDA-evoked dopamine release was reduced by increasing the perfusate concentration of Ca^2+ . On the other hand, α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (non-NMDA agonist)-evoked release and high K^+ (50 mM KCl)-evoked release of dopamine were unaffected under pentobarbital anesthesia. These results suggest that pentobarbital selectively inhibits the extracellular release of dopamine by activation of NMDA receptors, but not non-NMDA receptors in the striatum, and the inhibition of neurotransmitter release may, in part, contribute to the protective effect of pentobarbital on brain damage induced by ischemic brain injury.