Following transection of preganglionic autonomic nerves or in spinal cord injury, there are marked changes in the nerves that remain. Such changes can be manifested not only as nerve growth and changes in neurotransmitter expression but, remarkably, in reorganization of nerve pathways and their function. The most dramatic examples of such plasticity occur in the urogenital tract, and it is probable that the anatomical organization of nerve pathways in this region accounts for this (see Refs. 215-218) Not all preganglionic sympathetic nerves synapse with post-ganglionic neurons in the prevertebral or paravertebral ganglia. Thus, some of the sympathetic nerves traveling to the pelvic viscera in the hypogastric nerve are pre-ganglionic and also synapse with local ganglia in the pelvic region and the pelvic plexus. Since sprouting is a common response of the nerves that remain following nerve injury, the close association of the different divisions of the autonomic nervous system in the pelvic region opens up the possibility for new connections to form new pathways. Spinal cord injury can unmask spinal reflexes that are normally inhibited by input from higher centers in the brain (219). Spinal cord injury can also lead to changes in the sensory nerves supplying the bladder (220-222). Complete decentralization of the rat bladder by simultaneous transection of the hypogastric and pelvic nerves results in increased levels of NGF in the bladder (223). Since NGF acts predominantly on unmyelinated sensory nerves and sympathetic nerves, it could well play a role in plasticity following decentralization or spinal cord injury. These changes in sensory nerves and reflexes on spinal cord injury do not restore normal function. In many cases, detrusor-sphincter dyssyner-gia can occur (215,216). Plasticity of bladder afferents under pathological conditions may well contribute to bladder hyperactivity (216). Intravesical administration of capsaicin has been investigated with respect to the treatment of bladder hyperactivity (224,225).
Parasympathetic decentralization by either transection of the pelvic nerve or ventral roots in the cat has been shown to result in an increase of NA-containing nerves in the bladder and urethra (226-228). Similar changes have been found in human bladders from patients with sacral spinal cord lesions (229). In addition, the response to hypogastric nerve stimulation switches from the normal response of bladder contraction followed by relaxation to one of sustained bladder contraction after preganglionic parasympathetic denervation in cats (226,228). It has been suggested that denervation results in a switch in receptor expression from predominantly (3-adrenoceptors to predominantly a-adrenoceptors (226,227). VIP levels and VIP-containing nerve fibers also increase in the bladder after transec-tion of the pelvic nerves (230).
Increased expression of NA-containing nerves has also been observed in the striated muscle of the external urethral sphincter in humans following sacral spinal cord injury (231). Remarkably, experimental studies have shown that following somatic denervation there is sprouting of local autonomic nerves and reinnervation of motor endplates by autonomic cholinergic and/or adrenergic axons (232). Furthermore, removal of the somatic and parasympathetic input to the urethra results in a change of function such that sympathetic hypogastric nerve stimulation can result in activation of striated muscle fibres, a response that is never seen under normal conditions (233). Denervation may not be the only stimulus for auto-nomic plasticity in the bladder. Hypertrophy of the detrusor muscle and local inflammation can also induce changes in autonomic nerves under pathological conditions.
In the rat, under normal conditions, hypogastric nerve stimulation has no effect on penile pressure, which is controlled by the pelvic nerve. Following removal of the parasympathetic input by transection of the pelvic nerve, the pattern changes such that hypogastric nerve stimulation induces erection (234). Reorganization of autonomic pathways does not only occur after removal of parasympa-thetic input. After sympathetic decentralization in rats, pelvic nerve stimulation can cause contraction of the vas deferens, a response that normally can only be elicited by the hypogastric nerve (235). It has been proposed that decentralized local sympathetic postganglionic neurons are reinnervated by preganglionic axons in the pelvic nerve (235).
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