Dopaminergic regulation of mate competition aggression and aromatase-Fos colocalization in vasotocin neurons.

Dopaminergic regulation of mate competition aggression and aromatase-Fos colocalization in vasotocin neurons.
复制标题

催产素神经元中交配竞争攻击和芳香酶-Fos 共定位的多巴胺能调节。

DOI:
10.1016/j.neuropharm.2009.06.009
复制
发表时间:
2010
期刊:
影响因子:
4.7
通讯作者:
Goodson,JamesL
Goodson,JamesL
中科院分区:
医学2区
文献类型:
--
作者:
Kabelik,David;Kelly,AubreyM;Goodson,JamesL

文献摘要

相似文献

最近的实验表明,对潜在配偶的侵略性竞争涉及不同的神经机制比领土,居民入侵者的侵略。然而,尽管配偶竞争攻击的重要性显而易见,但我们对其调控知之甚少。立即早期基因实验表明,在领土的侵略,配偶竞争在雀类是伴随着与联系和动机,包括在内侧床核的终纹(BSTm)和中脑多巴胺(DA)神经元,项目的BSTm的催产素(VT)神经元的激活。虽然VT是已知的,以促进配偶竞争侵略,DA的作用以前没有被检查。我们现在表明,在雄性斑胸草雀(Taeniopygia guttata),配偶竞争侵略抑制D2激动剂quinpirole,虽然不是D1激动剂SKF-38393或D4激动剂PD 168077。D3受体激动剂7-OH-DPAT也能抑制攻击性,但仅在高剂量处理后才能抑制攻击性,这可能是通过与D2受体的非特异性结合而影响攻击性。在随后的实验中,中枢VT输注未能恢复D2激动剂抑制的攻击性,表明D2不通过抑制BSTm神经元VT释放来抑制攻击性。在最后的实验中,我们检测到D2激动剂诱导的立即早期基因c-fos和类固醇转化酶芳香酶(ARO)的VT神经元内的BSTm的免疫荧光共定位的产品的增加。因此,虽然VT和DA似乎独立地影响配偶竞争攻击,BSTm VT神经元明显受到D2受体激活的影响,这可能会改变未来的行为。
Recent experiments demonstrate that aggressive competition for potential mates involves different neural mechanisms than does territorial, resident-intruder aggression. However, despite the obvious importance of mate competition aggression, we know little about its regulation. Immediate early gene experiments show that in contrast to territorial aggression, mate competition in finches is accompanied by the activation of neural populations associated with affiliation and motivation, including vasotocin (VT) neurons in the medial bed nucleus of the stria terminalis (BSTm) and midbrain dopamine (DA) neurons that project to the BSTm. Although VT is known to facilitate mate competition aggression, the role of DA has not previously been examined. We now show that in male zebra finches (Taeniopygia guttata), mate competition aggression is inhibited by the D2agonist quinpirole, though not the D1agonist SKF-38393 or the D4agonist PD168077. The D3agonist 7-OH-DPAT also inhibited aggression, but only following high dose treatment that may affect aggression via nonspecific binding to D2receptors. Central VT infusion failed to restore D2agonist-inhibited aggression in a subsequent experiment, demonstrating that D2does not suppress aggression by inhibiting VT release from BSTm neurons. In a final experiment, we detected D2agonist-induced increases in immunofluorescent colocalization of the product of the immediate early gene c-fos and the steroid-converting enzyme aromatase (ARO) within VT neurons of the BSTm. Thus, although VT and DA appear to influence mate competition aggression independently, BSTm VT neurons are clearly influenced by the activation of D2receptors, which may modify future behaviors.