title: Somatotopic redistribution of c-fos expressing neurons in the superficial dorsal horn after peripheral nerve injury.
abstract: The functional somatotopic reorganization of the lumbar spinal cord dorsal horn after nerve injury was studied in the rat by mapping the stimulus-evoked distribution of neurons expressing proto-oncogene c-fos. In three different nerve injury paradigms, the saphenous nerve was electrically stimulated at C-fibre strength at survival times ranging from 40 h to more than six months: 1) Saphenous nerve stimulation from three weeks onwards after ipsilateral sciatic nerve transection resulted in an increase in the number of Fos-immunoreactive neurons within the dorsal horn saphenous territory in laminae I-II, and an expansion of the saphenous territory into the denervated sciatic territory until 14 weeks postinjury. 2) Saphenous nerve stimulation from five days onwards after ipsilateral sciatic nerve section combined with saphenous nerve crush resulted in an increase in the number of Fos-immunoreactive neurons within the dorsal horn saphenous nerve territory, and an expansion of the saphenous nerve territory into the denervated sciatic nerve territory. 3) Stimulation of the crushed nerve (without previous adjacent nerve section) at five days, but not at eight months resulted in a temporary increase in the number of Fos-immunoreactive neurons within the territory of the injured nerve, and no change in area at either survival time. The results indicate that nerve injury results in an increased capacity of afferents in an adjacent uninjured, or regenerating nerve, to excite neurons both in its own and in the territory of the permanently injured nerve in the dorsal horn. The onset and duration of the increased postsynaptic excitability and expansion depends on the types of nerve injuries involved. These findings indicate the complexity of the central changes that follows in nerve injuries that contain a mixture of uninjured, regenerating and permanently destroyed afferents.
authors.affiliation: Karolinska Institutet, Department of Neuroscience, Doktorsringen, Stockholm, Sweden.
authors.forename: C
authors.initials: C
authors.lastname: Molander
authors.forename: J
authors.initials: J
authors.lastname: Hongpaisan
authors.forename: P
authors.initials: P
authors.lastname: Shortland
mesh_terms: D000818:Animals; D003714:Denervation; D005260:Female; D006614:Hindlimb / Q000294:innervation; D008297:Male; D009409:Nerve Crush; D009474:Neurons / Q000378:metabolism*; D059348:Peripheral Nerve Injuries; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012584:Sciatic Nerve / Q000293:injuries; D013116:Spinal Cord / Q000378:metabolism* / Q000473:pathology*; D014018:Tissue Distribution; D014947:Wounds and Injuries / Q000378:metabolism* / Q000473:pathology
chemical_list: D016760:Proto-Oncogene Proteins c-fos