de Groat W C, Araki I, Vizzard M A, Yoshiyama M, Yoshimura N, Sugaya K, Tai C, Roppolo J R
Department of Pharmacology, University of Pittsburgh, School of Medicine, PA 15261, USA.
Behav Brain Res. 1998 May;92(2):127-40. doi: 10.1016/s0166-4328(97)00185-x.
The storage and periodic elimination of urine are dependent upon neural circuits in the brain and spinal cord that co-ordinate the activity of the urinary bladder, the urethra and the striated urethral sphincter. This study utilized anatomical, electrophysiological and pharmacological techniques to examine: (1) the organization of the parasympathetic excitatory reflex mechanisms that control the urinary bladder of the rat and the cat; and (2) the changes in these reflexes during postnatal development and after spinal cord injury. In normal adult cats and rats, the parasympathetic excitatory input to the bladder is dependent upon a spinobulbospinal reflex pathway that is activated by myelinated (Adelta) bladder afferents and that passes through an integrative center (the pontine micturition center, PMC) in the rostral brain stem. Transneuronal tracing studies using pseudorabies virus as well as physiological methods have revealed that the PMC is located in close proximity to the locus coeruleus. Single unit recordings indicate that neurons in the PMC respond to afferent input from the bladder and are excited prior to or during reflex bladder contractions. Glutamic acid is the major excitatory transmitter in the micturition reflex pathway. Glutamatergic transmission which is mediated by AMPA/kainate and NMDA receptors can be modulated by a variety of other transmitters. In neonatal animals, a spinal micturition reflex is activated by somatic afferent fibers from the perigenital region. This reflex is suppressed during postnatal development, but can be unmasked in adult animals following spinal cord injury. Spinal injury also causes the emergence of a spinal bladder-to-bladder reflex which in the cat is activated by capsaicin-sensitive C-fiber bladder afferents. Patch clamp studies in spinal cord slice preparations indicate that developmental and spinal cord injury induced plasticity in sacral parasympathetic reflex pathways is due in part to alterations in glutamatergic excitatory transmission between interneurons and preganglionic neurons. Changes in the electrical properties of bladder afferent pathways may also contribute to the reorganization of bladder reflexes in paraplegic animals.
尿液的储存和定期排出依赖于大脑和脊髓中的神经回路，这些神经回路协调膀胱、尿道和尿道横纹括约肌的活动。本研究利用解剖学、电生理学和药理学技术来研究：（1）控制大鼠和猫膀胱的副交感神经兴奋性反射机制的组织；（2）这些反射在出生后发育过程中和脊髓损伤后的变化。在正常成年猫和大鼠中，膀胱的副交感神经兴奋性输入依赖于一条脊髓-延髓-脊髓反射通路，该通路由有髓鞘的（Aδ）膀胱传入神经激活，并通过延髓头端的一个整合中枢（脑桥排尿中枢，PMC）。使用伪狂犬病病毒的跨神经元追踪研究以及生理学方法表明，PMC位于蓝斑附近。单细胞记录表明，PMC中的神经元对来自膀胱的传入输入有反应，并在反射性膀胱收缩之前或期间被激活。谷氨酸是排尿反射通路中的主要兴奋性递质。由AMPA/海人藻酸受体和NMDA受体介导的谷氨酸能传递可被多种其他递质调节。在新生动物中，来自生殖器周围区域的躯体传入纤维可激活脊髓排尿反射。这种反射在出生后发育过程中受到抑制，但在成年动物脊髓损伤后可能会显现出来。脊髓损伤还会导致脊髓膀胱-to-膀胱反射的出现，在猫中，该反射由对辣椒素敏感的C纤维膀胱传入神经激活。脊髓切片制备中的膜片钳研究表明，发育和脊髓损伤诱导的骶副交感神经反射通路可塑性部分归因于中间神经元和节前神经元之间谷氨酸能兴奋性传递的改变。膀胱传入通路电特性的变化也可能有助于截瘫动物膀胱反射的重组。
