Frye Cheryl A, Walf Alicia A, Petralia Sandra M
Department of Psychology, Life Sciences 1058, The University at Albany-SUNY, Albany, NY 12222, USA.
Behav Brain Res. 2006 Sep 25;172(2):286-93. doi: 10.1016/j.bbr.2006.05.014. Epub 2006 Jun 15.
In the ventral tegmental area (VTA), progestins have actions involving dopamine type 1-like receptors (D(1)) and gamma-aminobutyric acid (GABA)(A)/benzodiazepine receptor complexes (GBRs) for lordosis. Evidence suggests that D(1) and GBRs can have G-protein-mediated effects. We investigated if, in the VTA, inhibiting G-proteins prevents D(1)- and/or GBR-mediated increases in progestin-facilitated lordosis. Hamsters, with bilateral guide cannulae to the VTA, received systemic E(2) (10 microg) at hour 0 and progesterone (P, 250 microg) at hour 45. At hour 48, hamsters were pre-tested for lordosis and infused with the G-protein inhibitor, guanosine 5'-O-(2-thiodiphosphate) (GDP-beta-S, 50 microM/side), or 10% DMSO saline vehicle. Thirty minutes after initial infusions, hamsters were re-tested and then immediately infused with the D(1) agonist, SKF38393 (100 ng/side), the GBR agonist, muscimol (100 ng/side), or saline vehicle. Hamsters were post-tested for lordosis 30 min later. For rats, E(2) (10 microg) priming at hour 0 was followed by lordosis pre-testing at hour 44. After pre-testing, rats received infusions of GDP-beta-S or vehicle, followed by infusions of SKF38393, muscimol, or vehicle and then infusions of the neurosteroid, 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP, 100 or 200 ng/side), or beta-cyclodextrin vehicle. Rats were tested immediately after each infusion of SKF38393, muscimol or vehicle, as well as 10 and 60 min after 3alpha,5alpha-THP or vehicle infusions. Inhibiting G-proteins, in the VTA, reduced the ability of systemic P or intra-VTA SKF38393 or muscimol to facilitate lordosis of E(2)-primed hamsters. Blocking G-proteins, in the VTA, prevented SKF38393-, muscimol- and/or 3alpha,5alpha-THP-mediated increases in lordosis of E(2)-primed rats. Thus, progestins' actions in the VTA for lordosis that involve D(1) and/or GBRs may also include recruitment of G-proteins.
在腹侧被盖区(VTA),孕激素通过涉及多巴胺1型样受体(D(1))和γ-氨基丁酸(GABA)(A)/苯二氮䓬受体复合物(GBRs)来发挥促进脊柱前凸的作用。有证据表明,D(1)和GBRs可产生G蛋白介导的效应。我们研究了在VTA中抑制G蛋白是否能阻止D(1)和/或GBR介导的孕激素促进的脊柱前凸增加。给双侧植入VTA导向套管的仓鼠在第0小时注射全身剂量的雌二醇(E(2),10微克),并在第45小时注射孕酮(P,250微克)。在第48小时,对仓鼠进行脊柱前凸预测试,并向其注入G蛋白抑制剂5'-O-(2-硫代二磷酸)鸟苷(GDP-β-S,50微摩尔/侧)或10%二甲亚砜生理盐水载体。首次注射30分钟后,再次对仓鼠进行测试,然后立即向其注入D(1)激动剂SKF38393(100纳克/侧)、GBR激动剂蝇蕈醇(100纳克/侧)或生理盐水载体。30分钟后对仓鼠进行脊柱前凸后测试。对于大鼠,在第0小时用E(2)(10微克)进行预处理,然后在第44小时进行脊柱前凸预测试。预测试后,给大鼠注入GDP-β-S或载体,随后注入SKF38393、蝇蕈醇或载体,然后注入神经甾体5α-孕烷-3α-醇-20-酮(3α,5α-THP,100或200纳克/侧)或β-环糊精载体。在每次注入SKF38393、蝇蕈醇或载体后,以及在注入3α,5α-THP或载体后10分钟和60分钟,立即对大鼠进行测试。在VTA中抑制G蛋白会降低全身P或脑室内SKF38393或蝇蕈醇促进E(2)预处理仓鼠脊柱前凸的能力。在VTA中阻断G蛋白可阻止SKF38393、蝇蕈醇和/或3α,5α-THP介导的E(2)预处理大鼠脊柱前凸增加。因此,孕激素在VTA中通过D(1)和/或GBR发挥的促进脊柱前凸作用可能还包括募集G蛋白。