Abstract
In vivo microdialysis was used to study the effect of intracerebral administration of dopamine agonists on dynorphin B release in the striatum and substantia nigra of rats. The release of dopamine and GABA was also investigated. Administration of the dopamine D 1 agonist SKF 38393 (10–100 μM) into the striatum increased extracellular dynorphin B and GABA levels in the ipsilateral substantia nigra, in a concentration-dependent manner. After a short-lasting increase, nigral dopamine levels were significantly decreased after the highest concentration of striatal SKF 38393. An increase in striatal dynorphin B, GABA and dopamine levels was also observed. When SKF 38393 (10 μM) was administered into the substantia nigra, nigral dynorphin B and GABA, but not dopamine levels increased. No significant effects were observed on striatal levels. Administration of the dopamine D 2 agonist, quinpirole (100μM), into the striatum decreased dopamine levels in both striatum and substantia nigra, while no effect was observed on striatal or nigral dynorphin B and GABA levels. Quinpirole (10–100μM) given into the substantia nigra, decreased striatal dopamine levels in a concentration manner. In the nigra, a short-lasting increase in dopamine levels was observed following the highest concentration of nigral quinpirole (100μM). The effect was followed by a decrease in dopamine levels. No significant effects were observed on striatal or nigral dynorphin B and GABA levels. The results show that stimulation of D 1 receptors in striatum and substantia nigra leads to activation of the striatonigral dynorphin pathway. A parallel effect could also be seen on nigral GABA release. In contrast, D 2 receptor stimulation primarily leads to inhibition of the nigrostriatal dopamine pathway, probably via autoreceptors located on striatal dopamine terminals and on nigral dopamine dendrites.
Published Version
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