title: Modulation of low-affinity nerve growth factor receptor in injured adult rat spinal cord motoneurons.
abstract: Spinal and brainstem motoneurons of the adult rat reexpress low-affinity nerve growth factor receptor (LNGFR) and its mRNA after axotomy. We have previously reported the time courses of this reexpression after cut (no regeneration) or crush (followed by regeneration) of the sciatic nerve. We have shown that the length of the different phases of this reexpression (appearance, maintenance and disappearance) can vary according to the type of axotomy. With the present study we expand our previous data and describe and analyze the modulation the LNGFR expression in adult spinal cord motoneurons following different lesion paradigms. In one approach we have imposed three traumatic injuries that still allow regeneration of the sciatic nerve but with a different time course with respect to the crush injury (application of a silicone regeneration chamber, multiple crushes and delayed repair of ligated nerves). In a second approach, we have determined the capability of three toxic or metabolic injuries to induce LNGFR expression without any direct trauma of the nerve (experimental diabetogenesis, botulinum and alpha-bungarotoxin intoxication and 2,5-hexanedione intoxication). In a third approach, we have investigated the effect of the block of the axoplasmic transport on the LNGFR expression following different topical applications of vincristine combined with a nerve crush. The results we present are consistent with the idea that: (1) LNGFR immunoreactivity in adult motoneurons is expressed by motoneurons that are attending to an axonal outgrowth and not a generic signal of cellular damage or impairment of the motor function; (2) LNGFR expression in these motoneurons is related to and parallels the outgrowth process time frame, and (3) the signal/s that trigger and sustain this reexpression may be retrogradely transported from the periphery.
authors.affiliation: Department of Experimental Medicine and Biochemical Science, University of Perugia, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Rende
authors.forename: C
authors.initials: C
authors.lastname: Provenzano
authors.forename: P
authors.initials: P
authors.lastname: Tonali
mesh_terms: D000287:Administration, Topical; D000818:Animals; D001905:Botulinum Toxins / Q000633:toxicity; D002038:Bungarotoxins / Q000633:toxicity; D002452:Cell Count; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D003929:Diabetic Neuropathies / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006588:Hexanones / Q000633:toxicity; D008026:Ligation; D009046:Motor Neurons / Q000378:metabolism* / Q000473:pathology; D009409:Nerve Crush; D009416:Nerve Regeneration / Q000187:drug effects; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D019736:Prostheses and Implants; D051381:Rats; D017207:Rats, Sprague-Dawley; D017475:Receptors, Nerve Growth Factor / Q000096:biosynthesis*; D012584:Sciatic Nerve / Q000187:drug effects / Q000293:injuries; D012828:Silicones; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology*; D015854:Up-Regulation; D014750:Vincristine / Q000008:administration & dosage / Q000633:toxicity
chemical_list: D002038:Bungarotoxins; D006588:Hexanones; D009419:Nerve Tissue Proteins; D017475:Receptors, Nerve Growth Factor; D012828:Silicones; D014750:Vincristine; C011269:2,5-hexanedione; D001905:Botulinum Toxins