de Groat W C
Department of Pharmacology, Medical School, University of Pittsburgh, PA, USA.
Eur Urol. 1998;34 Suppl 1:2-5. doi: 10.1159/000052265.
This paper will review the central nervous control of the lower urinary tract.
Neuroanatomical, electrophysiological and pharmacological techniques have provided information about the neural circuitry and the neurotransmitters involved in the neural control of voiding.
Storage of urine is dependent in part upon spinal reflex mechanisms that activate sympathetic and somatic pathways to the urethral outlet as well as tonic inhibitory systems in the brain that suppress the parasympathetic outflow to the urinary bladder. Voiding is mediated by inhibition of sympathetic and somatic reflex pathways and activation of a spinobulbospinal parasympathetic reflex pathway passing through a micturition center in the rostral pons. Studies in animals indicate that glutamic acid is the major excitatory transmitter in the micturition reflex pathway and that a number of other transmitter mechanisms (noradrenergic, dopaminergic and GABAergic) modulate glutamatergic transmission. Damage to the brain or spinal cord can induce bladder hyperactivity by reducing central inhibitory mechanisms or by promoting a reorganization of spinal reflex pathways.
The central nervous regulation of the lower urinary tract is mediated by simple on-off switching circuits in the brain and spinal cord that are under voluntary control. Interruption of central inhibitory mechanisms can unmask primitive voiding reflexes that trigger bladder hyperactivity.
本文将综述下尿路的中枢神经控制。
神经解剖学、电生理学和药理学技术已提供了有关排尿神经控制中所涉及的神经回路和神经递质的信息。
尿液储存部分依赖于激活至尿道外口的交感和躯体通路的脊髓反射机制，以及抑制膀胱副交感神经传出的大脑紧张性抑制系统。排尿由交感和躯体反射通路的抑制以及通过延髓脑桥排尿中枢的脊髓-延髓-脊髓副交感反射通路的激活介导。动物研究表明，谷氨酸是排尿反射通路中的主要兴奋性递质，并且许多其他递质机制（去甲肾上腺素能、多巴胺能和γ-氨基丁酸能）调节谷氨酸能传递。脑或脊髓损伤可通过减少中枢抑制机制或促进脊髓反射通路的重组来诱发膀胱功能亢进。
下尿路的中枢神经调节由大脑和脊髓中受自主控制的简单开-关切换回路介导。中枢抑制机制的中断可揭示触发膀胱功能亢进的原始排尿反射。
