D2 inhibition of stimulated Fos immunoreactivity in cultured tyrosine hydroxylase-ir hypothalamic neurons.
D2 inhibition of stimulated Fos immunoreactivity in cultured tyrosine hydroxylase-ir hypothalamic neurons.
复制标题
D2 抑制培养的酪氨酸羟化酶-ir 下丘脑神经元中刺激的 Fos 免疫反应性。
DOI：
10.1016/0006-8993(94)90711-0
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发表时间：
1994
期刊：
影响因子：
2.9
通讯作者：
Morris,M
中科院分区：
文献类型：
--
作者：
Sim,LJ;Selley,DE;Tsai,KP;Morris,M
We have previously demonstrated that Fos immunoreactivity can be stimulated by KCI, forskolin or glutamate in cultured tyrosine hydroxylase-immunoreactive (TH-ir) hypothalamic neurons. The present study was performed to determine whether agents that regulate dopaminergic activity, particularly D1and D2receptor agonists, modulate the intracellular cascade leading to Fos expression. Dissociated hypothalamic cultures were prepared from neonatal rats. The cultures were treated with D1- or D2-specific agonists, followed by KCl, forskolin or glutamate. Cultures were fixed after 2 h and immunocytochemically stained for tyrosine hydroxylase and Fos. Pretreatment of the cultures with the D2agonist LY163502 inhibited KCl- and forskolin-stimulated Fos-ir in TH-ir neurons in a saturable dose-dependent manner. The maximal effective dose was 30 μM LY163502, which decreased Fos-ir by 23% in cultures treated with 50 mM KCl and by 33% in those treated with 30 μM forskolin. The D2agonist had no effect on glutamate-stimulated Fos-ir. LY163502 inhibition of Fos-ir was blocked by D2antagonist orBordetellapertussis toxin pretreatment which demonstrates that the effect is mediated by D2receptor activation of an inhibitory G protein. Treatment of the cultures with the D1agonist SKF82526 had no effect on basal or stimulated levels of Fos-ir. These results demonstrate that in neonatal TH-ir hypothalamic neurons the D2receptor system may regulate levels of the immediate-early gene product Fos and therefore, subsequent genetic expression in these neurons.
