Dornan W A, Vink K L, Malen P, Short K, Struthers W, Barrett C
Department of Psychology, Illinois Wesleyan University, Bloomington 61701.
Physiol Behav. 1993 Aug;54(2):249-58. doi: 10.1016/0031-9384(93)90107-q.
Accumulating evidence indicates that neurokinins play a role in the neural regulation of male rat copulatory behavior. We have previously reported that injections of the neurokinin substance P into the medial preoptic nucleus facilitated male rat copulatory behavior. Recently, a number of other neurokinins, neurokinin K (neuropeptide K), neurokinin A (substance K), and neurokinin gamma (derived from the same gene as substance P), have been identified in the mammalian CNS. Therefore, in a series of experiments we examined the effects on male copulatory behavior following bilateral injections of different doses of neurokinin K (NkK), neurokinin A (NkA), or neurokinin gamma (Nk gamma) into the medial preoptic area (MPOA), bed nucleus of the stria terminalis (BnST), or the caudate/putamen. Bilateral injections of NkK into the MPOA or BnST inhibited the expression of male copulatory behavior. The most marked effect was seen following bilateral injections of 0.25 and 0.52 nmol of NkK into the MPOA and the BnST. These injections produced a dramatic suppression of copulatory behavior in previously sexually vigorous male rats when compared to control injections. In contrast, bilateral injections of three different doses of NkA into the MPOA failed to affect any parameter of male copulatory behavior. Bilateral injections of 0.431 nmol of Nk gamma into the MPOA failed to affect the expression of copulatory behavior, but significantly delayed its initiation when compared to controls. Bilateral injections of 0.251 nmol of NkK into the caudate/putamen had no significant effect on copulatory behavior in sexually vigorous male rats when compared to control injections. The results of the present study provide further support for a role of neurokinins in the regulation of copulatory behavior in male rat. Taken together, these results suggest that the effects of neurokinins upon the expression of male copulatory behavior are site specific for brain regions in the sexually dimorphic vomeronasal pathway which includes the MeA, BnST, and MPOA.
越来越多的证据表明,神经激肽在雄性大鼠交配行为的神经调节中发挥作用。我们之前曾报道,向内侧视前核注射神经激肽P可促进雄性大鼠的交配行为。最近,在哺乳动物中枢神经系统中发现了许多其他神经激肽,如神经激肽K(神经肽K)、神经激肽A(物质K)和神经激肽γ(与物质P来自同一基因)。因此,在一系列实验中,我们研究了向内侧视前区(MPOA)、终纹床核(BnST)或尾状核/壳核双侧注射不同剂量的神经激肽K(NkK)、神经激肽A(NkA)或神经激肽γ(Nkγ)对雄性交配行为的影响。向MPOA或BnST双侧注射NkK会抑制雄性交配行为的表达。最显著的效果出现在向MPOA和BnST双侧注射0.25和0.52 nmol的NkK之后。与对照注射相比,这些注射使先前性活跃的雄性大鼠的交配行为受到显著抑制。相比之下,向MPOA双侧注射三种不同剂量的NkA未能影响雄性交配行为的任何参数。向MPOA双侧注射0.431 nmol的Nkγ未能影响交配行为的表达,但与对照相比,显著延迟了其开始时间。与对照注射相比,向尾状核/壳核双侧注射0.251 nmol的NkK对性活跃的雄性大鼠的交配行为没有显著影响。本研究结果为神经激肽在雄性大鼠交配行为调节中的作用提供了进一步支持。综上所述,这些结果表明,神经激肽对雄性交配行为表达的影响在性二态性犁鼻器通路的脑区中具有位点特异性,该通路包括内侧杏仁核、终纹床核和内侧视前区。