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Levodopoa but not bromocriptine induces AP-1 and creb DNA-binding activity in the dopamine-depleted striatum of the rat.
To elucidate the neurochemical mechanism that underlies the effect of anti-parkinsonian agents on motor activities in the dopamine-depleted striatum, we evaluated AP-I and CREB DNA-binding activity in the striatum of 6-hydroxydopamine-lesioned rats by use of a gel mobility-shift assay. Rats with a unilateral lesion of the nigrostriatal dopamine pathway were injected i.p. with either SKF38393 (a DI receptor agonist), bromocriptine (a D2 receptor agonist), or levodopa (a Dl/D2 receptor agonist). Each treatment increased the number of rotational responses of rats contralateral to the lesioned side. However, only SKF38393 and levodopa increased AP-I and CREB DNA-binding activity in the dopamine-depleted striatum. As with the expression of c-fos, supersensitive DI receptors may play a key role in the enhanced induction of AP-I and CREB DNA-binding activity in the dopamine-depleted striatum. Supershift analysis revealed that c-Fos; and Jun family proteins are the main components for AP-1 induced in the dopamine-depleted striaturn by SKF38393 or levodopa.[1]References
- Levodopoa but not bromocriptine induces AP-1 and creb DNA-binding activity in the dopamine-depleted striatum of the rat. Kashihara, K., Akiyama, K., Ishihara, T., Shiro, Y., Shohmori, T. Life Sci. (1996) [Pubmed]
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