Kostrzewa R M, Fukushima H, Harston C T, Perry K W, Fuller R W, Kastin A J
Brain Res Bull. 1979 Nov-Dec;4(6):799-802. doi: 10.1016/0361-9230(79)90015-7.
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.
由于抗帕金森病药物L-脯氨酰-L-亮氨酰-甘氨酸酰胺(PLG,MIF-I)对纹状体多巴胺(DA)周转的作用存在相互矛盾的报道,因此对这一过程进行了重新研究。在本系列研究中,发现我们的MIF-I(200 ng脑室内注射)和Versteeg等人[25]使用的MIF-I均不能有效改变用α-甲基-p-酪氨酸(300 mg/kg腹腔注射)预处理的大鼠尾状核中内源性DA下降的速率。此外,我们的MIF-I(1 mg/kg腹腔注射)并未改变大鼠纹状体中的内源性二羟基苯乙酸(DOPAC)或高香草酸(HVA)。这些研究表明,MIF-I不会改变黑质纹状体神经元中DA的周转率。MIF-I或由MIF-I释放的某些物质可能作用于突触后受体部位。