Department of Anatomy & Cell Biology, the University of Western Ontario, London, Ontario, Canada; Department of Physiology, University of Michigan, Ann Arbor, Michigan, United States of America.
Department of Anatomy & Cell Biology, the University of Western Ontario, London, Ontario, Canada; Department of Physiology, University of Michigan, Ann Arbor, Michigan, United States of America; Department of Neurobiology & Anatomical Sciences, University of Mississippi Medical Center, Jackson, Mississippi, United States of America; Department of Physiology & Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States of America.
PLoS One. 2015 Mar 31;10(3):e0121130. doi: 10.1371/journal.pone.0121130. eCollection 2015.
Ejaculation is controlled by a spinal ejaculation generator located in the lumbosacral spinal cord, consisting in male rats of lumbar spinothalamic (LSt) cells and their inter-spinal projections to autonomic and motor centers. LSt cells co-express several neuropeptides, including gastrin releasing peptide (GRP) and enkephalin. We previously demonstrated in rats that GRP regulates ejaculation by acting within the lumbosacral spinal cord. In the present study, the hypothesis was tested that enkephalin controls ejaculation by acting on mu (MOR) or delta opioid receptors (DOR) in LSt target areas. Adult male rats were anesthetized and spinalized and received intrathecal infusions of vehicle, MOR antagonist CTOP (0.4 or 4 nmol), DOR antagonist (TIPP (0.4, 4 or 40 nmol), MOR agonist DAMGO (0.1 or 10 nmol), or DOR agonist deltorphin II (1.3 or 13 nmol). Ejaculatory reflexes were triggered by stimulation of the dorsal penile nerve (DPN) and seminal vesicle pressure and rhythmic contractions of the bulbocavernosus muscle were analyzed. Intrathecal infusion of MOR or DOR antagonists effectively blocked ejaculatory reflexes induced by DPN stimulation. Intrathecal infusion of DAMGO, but not deltorphin II triggered ejaculation in absence of DPN stimulation. Both MOR and DOR agonists facilitated ejaculatory reflexes induced by subthreshold DPN stimulation in all animals. Overall, these results support the hypothesis that enkephalin plays a critical role in the control of ejaculation in male rats. Activation of either MOR or DOR in LSt target areas is required for ejaculation, while MOR activation is sufficient to trigger ejaculation in the absence of sensory stimulation.
射精是由位于腰骶脊髓的脊髓射精发生器控制的,在雄性大鼠中,该发生器由腰骶部的脊髓丘脑(LSt)细胞及其向自主和运动中枢的脊髓内投射组成。LSt 细胞共同表达几种神经肽,包括胃泌素释放肽(GRP)和脑啡肽。我们之前在大鼠中证明,GRP 通过在腰骶脊髓内发挥作用来调节射精。在本研究中,我们假设脑啡肽通过作用于 LSt 靶区的μ(MOR)或δ阿片受体(DOR)来控制射精。成年雄性大鼠麻醉并脊髓化,并接受鞘内输注载体、MOR 拮抗剂 CTOP(0.4 或 4 nmol)、DOR 拮抗剂(TIPP(0.4、4 或 40 nmol)、MOR 激动剂 DAMGO(0.1 或 10 nmol)或 DOR 激动剂 delta 啡肽 II(1.3 或 13 nmol)。通过刺激背阴茎神经(DPN)和精囊压力触发射精反射,分析球海绵体肌的节律性收缩。鞘内输注 MOR 或 DOR 拮抗剂可有效阻断 DPN 刺激引起的射精反射。鞘内输注 DAMGO,但不是 delta 啡肽 II,在没有 DPN 刺激的情况下引发射精。MOR 和 DOR 激动剂均促进所有动物亚阈刺激 DPN 刺激引起的射精反射。总的来说,这些结果支持这样的假设,即脑啡肽在雄性大鼠射精的控制中起着关键作用。LSt 靶区中 MOR 或 DOR 的激活是射精所必需的,而 MOR 的激活足以在没有感觉刺激的情况下引发射精。