SPROUTING OF PRIMARY AFFERENT-FIBERS AFTER SPINAL-CORD TRANSECTION INTHE RAT

After spinal cord injury, hyper-reflexia can lead to episodic hyperten sion, muscle spasticity and urinary bladder dyssynergia. This conditio n may be caused by primary afferent fiber sprouting providing new inpu t to partially denervated spinal interneurons, autonomic neurons and m otor neurons. However, conflicting reports concerning afferent neurite sprouting after cord injury do not provide adequate information to as sociate sprouting with hyper-reflexia. Therefore, we studied the effec t of mid-thoracic spinal cord transection on central projections of se nsory neurons, quantified by area measurements. The area of myelinated afferent arbors, immunolabeled by cholera toxin B, was greater in lam inae I-V in lumbar, but not thoracic cord, by one week after cord tran section. Changes in small sensory neurons and their unmyelinated fiber s, immunolabeled for calcitonin gene-related peptide, were assessed in the cord and in dorsal root ganglia. The area of calcitonin gene-rela ted peptide-immunoreactive fibers in laminae III-V increased in all co rd segments at two weeks after cord transection, but not at one week. Numbers of sensory neurons immunoreactive for calcitonin gene-related peptide were unchanged, suggesting that the increased area of immunore activity reflected sprouting rather than peptide up-regulation. Immuno reactive fibers in the lateral horn increased only above the lesion an d in lumbar segments at two weeks after cord transection. They were no t continuous with dorsal horn fibers, suggesting that they were not pr imary afferent fibers. Using the fluorescent tracer DiI to label affer ent fibers, an increase in area could be seen in Clarke's nucleus caud al to the injury two weeks after transection. In conclusion, site-and time-dependent sprouting of myelinated and unmyelinated primary affere nt fibers, and possibly interneurons, occurred after spinal cord trans ection. Afferent fiber sprouting did not reach autonomic or motor neur ons directly, but may cause hyper-reflexia by increasing inputs to int erneurons. (C) 1998 IBRO. Published by Elsevier Science Ltd.