Distinct Expression of c-Jun and HSP27 in Axotomized and Spared Bulbospinal Neurons After Cervical Spinal Cord Injury

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In several populations of adult central nervous system neurons, axon damage can lead to an up-regulation of some transcription factors among which is c-Jun, known to be a key regulator of neuron cell body response to injury and of its intrinsic potential for axon regeneration. Thus, cervical spinal hemisection leads to c-Jun up-regulation in bulbospinal and rubrospinal axotomized neurons. The aims of the present study were to specify, after a unilateral cervical spinal cord injury, the expression of another marker of the neuronal stress response, heat shock protein 27 (HSP27) in axotomized neurons of the medulla (labeled by fluorogold retrograde tracer), and to compare it to that of c-Jun. In the medulla of injured rats, HSP27 and phospho-HSP27 were expressed in sub-populations of axotomized neurons, principally in the rostral ventral respiratory group (rVRG) (20%), the dorsal part of the gigantocellularis (Gi) (50%), and vestibular nucleus, but seldom in the ventral Gi and raphe nucleus, indicating a heterogeneous post-lesion cell body response between these different neuron populations. By contrast, phospho-c-Jun was up-regulated in axotomized neurons in all nuclei containing bulbospinal neurons, including the rVRG and Gi. In these areas, phospho-c-Jun was also up-regulated in uninjured bulbospinal neurons which project caudal to the spinal cord injury (labeled by fluorogold retrograde tracer). In contrast to phospho-c-Jun, HSP27 immunoreactivity was generally not present in neurons with spared axons. Our results show that various bulbospinal neuron populations react differentially to the injury and that spinal cord injury affects also bulbospinal neurons that are spared by the injury. However, the molecular cell body response of spared neurons is distinct from that of axotomized neurons since they can up-regulate c-Jun but not HSP27.