Abstract：
Motivation-driven mating is a basic affair for the maintenance of species. However, the underlying molecular mechanisms that control mating motivation are not fully understood. Here, we report that NRG1-ErbB4 signaling in the medial amygdala (MeA) is pivotal in regulating mating motivation. NRG1 expression in the MeA negatively correlates with the mating motivation levels in adult male mice. Local injection and knockdown of MeA NRG1 reduce and promote mating motivation, respectively. Consistently, knockdown of MeA ErbB4, a major receptor for NRG1, and genetic inactivation of its kinase both promote mating motivation. ErbB4 deletion decreases neuronal excitability, whereas chemogenetic manipulations of ErbB4-positive neuronal activities bidirectionally modulate mating motivation. We also identify that the effects of NRG1-ErbB4 signaling on neuronal excitability and mating motivation rely on hyperpolarization-activated cyclic nucleotide-gated channel 3. This study reveals a critical molecular mechanism for regulating mating motivation in adult male mice.
摘要：
动机驱动的交配是维持物种的基本事务。然而,控制交配动机的潜在分子机制尚未完全了解。这里,我们报告说，内侧杏仁核（MeA）中的NRG1-ErbB4信号在调节交配动机中至关重要。MeA中NRG1的表达与成年雄性小鼠的交配动机水平呈负相关。局部注射和敲除MeANRG1减少和促进交配动机，分别。始终如一，NRG1的主要受体MeAErbB4的敲除及其激酶的遗传失活都促进了交配动机。ErbB4缺失降低神经元兴奋性，而ErbB4阳性神经元活动的化学遗传学操作双向调节交配动机。我们还发现NRG1-ErbB4信号对神经元兴奋性和交配动机的影响依赖于超极化激活的环核苷酸门控通道3。这项研究揭示了调节成年雄性小鼠交配动机的关键分子机制。
