AXONAL REGENERATION AND PHYSIOLOGICAL-ACTIVITY FOLLOWING TRANSECTION AND IMMUNOLOGICAL DISRUPTION OF MYELIN WITHIN THE HATCHLING CHICK SPINAL-CORD

Transections of the chicken spinal cord after the developmental onset of myelination at embryonic day (E) 13 results in little or no functio nal regeneration. However, intraspinal injection of serum complement p roteins with complement-binding GalC or 04 antibodies between E9-E12 r esults in a delay of the onset of myelination until E17. A subsequent transection of the spinal cord as tate as E15 (i.e., during the normal restrictive period for repair) results in neuroanatomical regeneratio n and functional recovery. Utilizing a similar immunological protocol, we evoked a transient alteration of myelin structure in the posthatch ing (P) chicken spinal cord, characterized by widespread ''unravelling '' of myelin sheaths and a loss of MBP immunoreactivity (myelin disrup tion). Myelin repair began within 7 d of cessation of the myelin disru ption protocol. Long term disruption of thoracic spinal cord myelin wa s initiated after a P2-P10 thoracic transection and maintained for >14 d by intraspinal infusion of serum complement proteins plus complemen t-binding GalC or 04 antibodies. Fourteen to 28 d later, retrograde tr act tracing experiments, including double-labeling protocols, indicate d that approximately 6-19% of the brainstem-spinal projections had reg enerated across the transection site to lumbar levels. Even though vol untary locomotion was not observed after recovery, focal electrical st imulation of identified brainstem locomotor regions evoked peripheral nerve activity in paralyzed preparations, as well as leg muscle activi ty patterns typical of stepping in unparalyzed animals. This indicated that a transient alteration of myelin structure in the injured adult avian spinal cord facilitated brainstem-spinal axonal regrowth resulti ng in functional synaptogenesis with target neurons.