Lesion induced expression of low-affinity NGF-binding protein (p75) immunoreactivity after neonatal and adult aspiration lesions of the rat dorsomedial prefrontal cortex.
The present study was performed in order to examine whether or not NGF-mediated processes could be involved in the sparing of function observed after neonatal prefrontal cortex lesions. After unilateral neonatal aspiration lesions of the dorsomedial prefrontal cortex, fibers immunoreactive for the low-affinity NGF-binding protein (p75) with a deviant morphology were observed in the severed hemisphere only. The morphology of these fibers was characterized by their large caliber, their large, often bulbous varicosities, and their curly appearance. These fibers were present as soon as 24 h after the operation. Between 3 and 5 days after the operation, the greatest abundance of these fibers was found in the ventrorostral areas of the forebrain and along the pathways of cortical projections of the cholinergic cell groups. After 7 days, such fibers were no longer observed. After comparable lesions in adult animals, a similar type of fiber was observed in the lesioned hemisphere. However, in these cases a response comparable to that observed in the neonatal animals was not observed until 5 days after the operation, with fewer fibers. Furthermore, in contrast to what was observed after neonatal lesions, in adult animals no indications of retrograde transport of p75 immunoreactive material towards the cholinergic cells of the basal forebrain nuclei were found. From these findings it was concluded that the prompt upregulation of p75 expression in neonatal animals may contribute to the survival of the cholinergic cells of the basal forebrain, and may therefore be involved in the restoration of function of the medial prefrontal cortex.
Netherlands Institute for Brain Research, Graduate School Neurosciences Amsterdam.
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CG
van Eden
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Rinkens
D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D005260:Female; D007839:Functional Laterality; D007150:Immunohistochemistry; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis / Q000378:metabolism*; D009412:Nerve Fibers / Q000378:metabolism / Q000473:pathology; D009416:Nerve Regeneration; D017397:Prefrontal Cortex / Q000254:growth & development / Q000378:metabolism* / Q000473:pathology; D016548:Prosencephalon / Q000254:growth & development / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000032:analysis / Q000378:metabolism*; D013997:Time Factors
D008562:Membrane Glycoproteins; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor