Dopamine autoreceptor stimulation increases protein carboxyl methylation in striatal slices.

摘要: : We have investigated the possibility that protein carboxyl methylation is involved in coupling dopamine autoreceptor stimulation to intracellular events such as inhibition of synthesis or release. The agonists apomorphine and TL-99 were found stimulate methyl ester formation striatal slices preloaded with [3H]methionine. stimulatory effects dose-dependent, not due changes [3H]methionine uptake S-[3H]-adenosyl-methionine formation, blocked by stereospecific antagonist (+)-butaclamol. Stimulation readily observed only when are prepared from rats pretreated reserpine deplete endogenous brain catecholamines. This suggests normal (DA) released during slice preparation incubation masks produced exogenously administered on methylase (PCM) activity. Additional experiments suggested mediated via an interaction DA autoreceptors rather than postsynaptic receptors. Destruction monoamine neurons their associated injecting 6-hydroxydopamine into area medial forebrain bundle abolished slices. Furthermore putative selective agonist EMD 23 448 was also These findings, discussed terms calcium-dependent functions, support hypothesis PCM may be a key component biochemical transduction stimulation.