Neural plasticity relating to micturitinal disorder and its recovery in rats with injury to the central nervous system.

1.部分去脑致微神经元障碍及其康复。额叶皮质部分内侧去脑或外侧去脑分别引起膀胱体积增大或减小。然而，部分去脑后两周，膀胱容量恢复到去脑前的容量。结论：1.桥脑排尿中枢的HRP法、神经生长因子、c-fos、c-fos-mRNA、NSE-mRNA阳性神经元的分布均不能反映其恢复过程。脊髓背索损伤致排尿障碍及其康复。中脑去脑猫，背索损伤不影响反射性排尿。慢性脊髓损伤后，单次排尿量减少，膀胱感觉消失，2周后恢复。虽然膀胱感觉的上行通路是背侧系统和脊髓丘脑束，但背侧系统可能是主要通路，脊髓丘脑束可能成为背侧系统的作用 关于我们 l系统受到伤害时。脊髓损伤后尿潴留及其康复。用毛细管电泳法测定腰骶髓谷氨酸、甘氨酸、γ-氨基丁酸含量。鞘内注射谷氨酸增加大鼠腰骶髓中的甘氨酸。在急性脊髓损伤大鼠中，腰骶髓中的谷氨酸和甘氨酸增加，鞘内注射谷氨酸受体拮抗剂减少甘氨酸。因此，脊髓谷氨酸神经元可能是被来自上中枢神经系统的输入抑制的自激活神经元。当来自上中枢神经系统的输入因脊髓损伤而消失时，自激活的谷氨酸神经元可促进甘氨酸神经元，甘氨酸神经元可抑制除支配外尿道括约肌的Onuf神经元之外的自主神经元和运动神经元。在慢性脊髓损伤大鼠中，腰骶髓中的谷氨酸和甘氨酸减少，表明甘氨酸神经元活动可能通过谷氨酸神经元活动的减少而减少，并且可能发生脊髓反射亢进。少

1. Miclurihional disorder by partial decerebrae and its recovery. Partial inside or outside decerebrate of the frontal cortex induced large or small bladder volume, respectively. Twe weeks after partial decerebrate, however, bladder volume returned to the volume before decerebrate. Its recovery process could not be revealed by HRP study into the pontine micturition cenler, or distributions of positive neurons of nerve growth facter, c-fos, c-fos-mRNA, or NSE-mRNA.2. Micturitional disorder by dorsal funiculus injury and its reco very. In mid-brain decerebrate cats, dorsal funiculus injury did not influence the reflex micturition. In chronic cat with dorsal funiculus injury, single micturition volume decreased, and bladder sensation disappeared, but recovered 2 weeks after its injury. Although ascending pathways of bladder sensation are the dorsal system and spinotlialamic tract, the dorsal system may be the main pathway, and the spinothalamic tract may become to play a role of the dorsa … More l system when it is injured.3. Urinary retention by spinal cord injury and its recovery. Glutamate, aspartare, glycine and GABA in the lumbosacral spinal cord were measured by capillary electrophoresis. Intrathecal injection of glutamate increased glycine in the lumbosacral cord in rats. In acute spinal rats, glutamate and glycine increased in the lumbosacral cord, and intrathecal injection of glutamate receptor antagonist decreased glycine. Therefore, spinal glutamate neurons may be autoactivating neurons which are inhibited by the input from the upper central nervous system. When the input from the upper central nervous system disappears by spinal cord injury, autoactivating glutamate neurons may facilitate glycine neurons which may inhibit autonomic neurons and motoneurons except for Onuf's neurons innervating the external urethral sphincter muscle. In chronic spinal rats, glutamate and glycine in the lumbosacral cord decreased, suggesting that glycine neuronal activity may decrease by the decrease of glutamate neuronal activity, and that spinal hyper-reflexia may occur. Less