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

1. 部分失智性微神经障碍及其恢复。额叶皮质部分内、外脱脑分别引起膀胱体积增大或减小。然而，在部分去脑后两周，膀胱容量恢复到去脑前的容量。其恢复过程不能通过HRP对脑桥排尿中枢的研究，也不能通过神经生长因子、c-fos、c-fos- mrna或nse - mrna阳性神经元的分布来揭示。背索损伤所致的排尿障碍及其恢复。中脑失智猫的背索损伤不影响反射性排尿。慢性背索损伤猫单次排尿量减少，膀胱感觉消失，损伤后2周恢复。虽然膀胱感觉的上升通路为背系和脊髓束，但背系可能是主要通路，脊髓丘脑束损伤后可能成为背系的辅助通路。脊髓损伤所致尿潴留及其恢复。用毛细管电泳法测定腰骶脊髓中谷氨酸、天冬氨酸、甘氨酸和GABA的含量。鞘内注射谷氨酸增加了大鼠腰骶束中的甘氨酸。急性脊髓大鼠腰骶脊髓谷氨酸和甘氨酸升高，鞘内注射谷氨酸受体拮抗剂可降低甘氨酸。因此，脊髓谷氨酸神经元可能是受上中枢神经系统输入抑制的自激活神经元。当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自主神经元和运动神经元，但支配尿道外括约肌的Onuf神经元除外。慢性脊髓大鼠腰骶束谷氨酸和甘氨酸减少，提示甘氨酸神经元活性可能因谷氨酸神经元活性降低而降低，可能发生脊髓反射过度。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