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首页> 外文期刊>Progress in brain research >Neurochemical plasticity and the role of neurotrophic factors in bladder reflex pathways after spinal cord injury.
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Neurochemical plasticity and the role of neurotrophic factors in bladder reflex pathways after spinal cord injury.

机译：脊髓损伤后神经化学可塑性和神经营养因子在膀胱反射途径中的作用。

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Transection of the spinal cord that interrupts the spinobulbospinal micturition reflex pathway, abolishes voluntary voiding and initially produces an areflexic bladder with complete urinary retention. However, depending upon the species, reflex bladder activity slowly recovers over the course of weeks or months. In chronic spinal animals, reflex mechanisms in the lumbosacral spinal cord are capable of duplicating many of the functions performed by reflex pathways in animals with an intact spinal cord and can induce bladder hyperreflexia. However, the bladder does not empty efficiently due to a loss of bladder-sphincter coordination (bladder-sphincter dyssynergia). In contrast to normal animals in which the sphincter relaxes during voiding, animals with a spinal cord injury exhibit sphincter contractions during voiding, an increase in urethral outlet resistance, urinary retention, bladder hyperreflexia, bladder overdistension, and an increase in bladder afferent cell size. Changes in electrophysiological or neurochemical properties of bladder afferent cells in the dorsal root ganglia and of spinal pathways could contribute to the emergence of the spinal micturition reflex, bladder hyperreflexia and changes in the pharmacologic responses of reflex pathways in the lumbosacral spinal cord after spinal cord injury. Urinary bladder hyperreflexia after spinal cord injury may reflect a change in the balance of neuroactive compounds in bladder reflex pathways. This review will detail: (1) changes in the neurochemical phenotype of bladder afferent neurons and of spinal neurons mediating micturition reflexes after spinal cord injury, with an emphasis on three neuroactive compounds, neuronal nitric oxide synthase (nNOS), galanin, and pituitary adenylate cyclase activating polypeptide (PACAP); (2) possible functional consequences on bladder reflexes of changes in spinal cord neurochemistry after spinal cord injury, and (3) the potential role of neurotrophic factors expressed in the urinary bladder orspinal cord after spinal cord injury in mediating these neurochemical changes.
机译：脊髓的横断会中断脊柱脊髓脊髓排尿反射通路，消除自愿排尿，并最初产生具有完全尿retention留的曲挠性膀胱。但是，根据物种的不同，反射膀胱活动会在数周或数月的时间内缓慢恢复。在慢性脊髓动物中，腰ac脊髓的反射机制能够复制具有完整脊髓的动物中反射途径所执行的许多功能，并且可以诱发膀胱反射亢进。但是，由于失去了膀胱括约肌的协调性（膀胱括约肌功能失调），膀胱不能有效排空。与在排尿期间括约肌松弛的正常动物相比，患有脊髓损伤的动物在排尿期间表现出括约肌收缩，尿道出口阻力增加，尿retention留，膀胱过度反射，膀胱过度扩张以及膀胱传入细胞大小增加。脊髓损伤后背根神经节和脊髓途径中膀胱传入细胞的电生理或神经化学性质的变化可能有助于出现排尿反射，膀胱反射亢进以及腰s部脊髓反射途径的药理反应变化。脊髓损伤后的膀胱反射亢进可能反映了膀胱反射通路中神经活性化合物平衡的变化。这篇综述将详细介绍：（1）脊髓损伤后膀胱传入神经元和介导排尿反射的脊髓神经元的神经化学表型的变化，重点是三种神经活性化合物，即神经元一氧化氮合酶（nNOS），甘丙肽和垂体腺苷酸环化酶激活多肽（PACAP）; （2）脊髓损伤后脊髓神经化学变化对膀胱反射的可能功能影响，以及（3）脊髓损伤后膀胱或脊髓中表达的神经营养因子在介导这些神经化学变化中的潜在作用。

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