Kato Ryuichi, Kiryu-Seo Sumiko, Sato Yoshikazu, Hisasue Shinichi, Tsukamoto Taiji, Kiyama Hiroshi
Department of Anatomy and Neurobiology, Graduate School of Medicine, Osaka City University, 1-4-3 Asahimachi, Abeno-ku, Osaka 545-8585, Japan.
Brain Res. 2003 Oct 3;986(1-2):166-73. doi: 10.1016/s0006-8993(03)03249-9.
Recovery of erectile dysfunction after cavernous nerve injury takes a long period. To elucidate this mechanism, unilateral cavernous nerve of male rat was cut, and the expression level of a nerve regeneration marker, the growth associated protein-43 (GAP-43) mRNA was evaluated by in situ hybridization and RT-PCR. While GAP-43 mRNA expression was transiently increased in the injured neurons of the major pelvic ganglion (MPG) at 7 days after nerve injury, continuous increase of GAP-43 mRNA was observed in the contralateral MPG from 7 days to 6 months after the nerve injury. Histochemical double-labeling studies for either neuronal NOS (nNOS) or tyrosine hydroxylase (TH) and the GAP-43 mRNA expression demonstrated that in injured MPG the transient up-regulation of GAP-43 mRNA was mainly seen in nNOS negative and/or TH positive neurons, suggesting non-parasympathetic post-ganglionic neurons, and also demonstrated that in contralateral MPG GAP-43 mRNA positive neurons were gradually increased in nNOS positive but TH negative neurons, suggesting parasympathetic post-ganglionic neurons. When a retrograde tracer Fluorogold (FG) was injected into the penile crus 7 days before histological experiments, FG-positive neurons were, if any, hardly seen in nNOS-positive neurons of the injured MPG for at least 6 months, whereas numerous FG-positive cells were seen in nNOS-positive neurons of the contralateral MPG. These results suggest that post-ganglionic projecting neurons of the intact side, which express increased GAP-43 mRNA, would be most likely to contribute to the recovery of the erectile function after unilateral cavernous nerve injury possibly by a plastic change such as nerve sprouting.
海绵体神经损伤后勃起功能障碍的恢复需要很长时间。为阐明这一机制，切断雄性大鼠的单侧海绵体神经，通过原位杂交和逆转录-聚合酶链反应（RT-PCR）评估神经再生标志物生长相关蛋白43（GAP-43）mRNA的表达水平。神经损伤后7天，主要盆腔神经节（MPG）受损神经元中GAP-43 mRNA表达短暂增加，而在神经损伤后7天至6个月，对侧MPG中GAP-43 mRNA持续增加。对神经元型一氧化氮合酶（nNOS）或酪氨酸羟化酶（TH）与GAP-43 mRNA表达进行组织化学双重标记研究表明，在受损的MPG中，GAP-43 mRNA的短暂上调主要见于nNOS阴性和/或TH阳性神经元，提示为非副交感神经节后神经元，同时也表明在对侧MPG中，GAP-43 mRNA阳性神经元在nNOS阳性但TH阴性的神经元中逐渐增加，提示为副交感神经节后神经元。在组织学实验前7天将逆行示踪剂荧光金（FG）注入阴茎脚，在至少6个月内，受损MPG的nNOS阳性神经元中几乎未见FG阳性神经元，而在对侧MPG的nNOS阳性神经元中可见大量FG阳性细胞。这些结果表明，完整侧表达增加的GAP-43 mRNA的节后投射神经元很可能通过神经发芽等可塑性变化，促进单侧海绵体神经损伤后勃起功能的恢复。
