Striatal dopamine turnover and MIF-I.
Because of conflicting reports of the actions of the antiparkinsonian agent L-prolyl-L-leucyl-glycine amide (PLG, MIF-I) on the turnover of striatal dopamine (DA), this process was reinvestigated. In the present series of studies, it was found that neither our MIF-I (200 ng ICV) nor the MIF-I used by Versteeg et al. [25] was effective in altering the rate of decline of endogenous DA in the caudate nucleus of rats pretreated with alpha-methyl-p-tyrosine (300 mg/kg IP). In addition, our MIF-I (1 mg/kg IP) did not change endogenous dihydroxyphenylacetic acid (DOPAC) or homovanillic acid (HVA) in rat striatum. These studies indicate that MIF-I does not alter the turnover rate of DA in nigrostriatal neurons. It is possible that MIF-I or some substance released by MIF-I acts at a postsynaptic receptor site.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D000978:Antiparkinson Agents / Q000494:pharmacology*; D002421:Caudate Nucleus / Q000187:drug effects; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D006719:Homovanillic Acid / Q000378:metabolism; D007276:Injections, Intraventricular; D009075:MSH Release-Inhibiting Hormone / Q000494:pharmacology*; D008297:Male; D051381:Rats
D000978:Antiparkinson Agents; D015102:3,4-Dihydroxyphenylacetic Acid; D009075:MSH Release-Inhibiting Hormone; D004298:Dopamine; D006719:Homovanillic Acid