The purpose of this study was to determine whether new descending brain-spinal cord projections are added with age in larval lamprey and might contribute substantially to restoration of these projections following spinal cord injury. Retrograde horseradish peroxidase (HRP) labeling of descending brain neurons was performed in "young" and "old" larval lamprey that differed in age by at least one year. In old larval lamprey, significantly more descending brain neurons projected to specific rostral levels of the spinal cord than in young animals. Furthermore, in young and old lamprey, the main morphological change in Müller and Mauthner cells was an increase in soma size. The major conclusion from the present study is that in larval lamprey, some new brain-spinal cord projections are added with age that could be due to axonal elongation by preexisting brain neurons and/or descending projections from new neurons (i.e., neurogenesis or maturation of incompletely differentiated neurons). Following spinal cord transections, the numbers of descending projections were not significantly different than those in normal, unlesioned animals. Thus, some new descending projections are added with age, but at a relatively slow rate, and the rate does not appear to be affected significantly by spinal cord transections. Together, the present results and those from our recent double-labeling study suggest that following spinal cord transection in larval lamprey, axonal regeneration by descending brain neurons, rather than the relatively slow addition of new brain-spinal cord projections with age, probably accounts for the majority of restored projections and recovery of locomotor function
In larval lamprey, with increasing recovery times after a transection of the rostral spinal cord, there is a gradual recovery of locomotor behavior, and descending brain neurons regenerate their axons for progressively greater distances below the transection site. In the present study, spinal cord "conditioning lesions" (i.e., transections) were performed in the spinal cord at 30% body length (BL; normalized distance from the head) or 50% BL. After various "lesion delay times" (D), a more proximal spinal cord "test lesion" (i.e., transection) was performed at 10% BL, and then, after various recovery times (R), horseradish peroxidase was applied to the spinal cord at 20% BL to determine the extent of axonal regeneration of descending brain neurons. Conditioning lesions at 30% BL, lesion delay times of 2 weeks, and recovery times of 4 weeks (D-R = 2-4 group) resulted in a significant enhancement of axonal regeneration for the total numbers of descending brain neurons as well as neurons in certain brain cell groups compared to control animals without conditioning lesions. Experiments with hemiconditioning lesions, which reduce interanimal variability, confirmed that conditioning lesions do significantly enhance axonal regeneration and indicate that axotomy rather than diffusible factors released at the injury site is primarily involved in this enhancement. Results from the present study suggest that conditioning lesions "prime" descending brain neurons via cell body responses and enhance subsequent axonal regeneration, probably by reducing the initial delay and/or increasing the initial rate of axonal outgrowth. Indexing termsaxotomy; reticulospinal neurons; spinal cord injury; conditioning lesion; test lesion When neurons are axotomized, they often are "primed" for possible subsequent axonal regeneration. If the axons of these neurons then receive a second "test lesion," often proximal to the first "conditioning lesion" (CL), regeneration can be enhanced compared with that of neurons without previous CLs. This phenomenon of enhanced axonal regeneration is called the "CL effect" (Forman et al., 1980). Because most studies of CL effects have been performed on nerves (e.g., sciatic nerve or optic nerve), crush injuries usually are employed for both the conditioning and the test lesions.After an initial CL, there are a series of morphological, physiological, and biochemical changes in axotomized neurons (McQuarrie and Grafstein, 1982;Redshaw and Bisby, 1987 Perry et al., 1987;Jacob and McQuarrie, 1991;Tetzlaff et al., 1996). Investigating the effects of CLs potentially might clarify the mechanisms that regulate neural regeneration, and it might then be possible to manipulate these mechanisms to enhance axonal regeneration. For example, a CL of the peripheral branch of neurons in dorsal root ganglia (DRG) raises cAMP levels and promotes axonal regeneration of the central branches of these neurons, and this effect can be mimicked by injection of cAMP in DRG (Qiu et al., 2002).The effects of CLs have been invest...
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