Dissociation of p75 receptors and nerve growth factor neurotrophic effects: lack of p75 immunoreactivity in striatum following physical trauma, excitotoxicity and NGF administration

Bartus, Raymond T.; Dean, Reginald L.; Abelleira, Susan M.; Charles, Vinod; Kordower, Jeffrey H.

doi:10.3233/rnn-1996-10107

Cited by 4 publications

(1 citation statement)

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“…In support of this concept, studies reported the de novo expression of p75 NTR within neurons of the adult rodent basal ganglia (Gage et al, 1989) either by the infusion of NGF into the striatum, striatal damage alone. On the other hand, a recent study failed to visualize p75 NTR ‐ir neurons 2 weeks after a variety of experimental manipulations, including NGF infusion, striatal damage, and excitotoxic lesions with QA (Bartus et al, 1996). In this regard, the present study revealed p75 NTR within striatal neurons after QA and 3‐NP lesions.…”

Section: Discussionmentioning

confidence: 99%

Excitotoxic and metabolic damage to the rodent striatum: Role of the P75 neurotrophin receptor and glial progenitors

Hanbury

Charles

Chen

et al. 2002

J of Comparative Neurology

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After injury, the striatum displays several morphologic responses that may play a role in both regenerative and degenerative events. One such response is the de novo expression of the low-affinity p75 neurotrophin receptor (p75(NTR)), a gene that plays critical roles in central nervous system (CNS) cell death pathways. The present series of experiments sought to elucidate the cellular origins of this p75(NTR) response, to define the conditions under which p75(NTR) is expressed after striatal injury, and how this receptor expression is associated with neuronal plasticity. After chemical lesions, by using either the excitotoxin quinolinic acid (QA) or the complex II mitochondria inhibitor 3-nitropropionic acid (3-NP), we compared the expression of the p75(NTR) receptor within the rat striatum at different survival times. Intrastriatal administration of QA between 7 days and 21 days postlesion induced p75(NTR) expression in astrocytes that was preferentially distributed throughout the lesion core. P75(NTR) immunoreactivity within astrocytes was seen at high (100-220 nmol) but not low (50 nmol) QA doses. Seven and 21 days after 3-NP lesions, p75(NTR) expression was present in astrocytes at all doses tested (100-1,000 nmol). However, in contrast to QA, these cells were located primarily around the periphery of the lesion and not within the lesion core. At the light microscopic level p75(NTR) immunoreactive elements resembled vasculature: but did not colocalize with the pan endothelium cell marker RecA-1. In contrast, p75(NTR)-containing astrocytes colocalized with nestin, vimentin, and 5-bromo-2-deoxyuridine, indicating that these cells are newly born astrocytes. Additionally, striatal cholinergic neurons were distributed around the lesion core expressed p75(NTR) 3-5 days after lesion in both QA and 3-NP lesions. These cells did not coexpress the pro-apoptotic degradation enzyme caspase-3. Taken together, these data indicate that striatal lesions created by means of excitotoxic or metabolic mechanisms trigger the expression of p75(NTR) in structures related to progenitor cells. The expression of the p75(NTR) receptor after these chemical lesions support the concept that this receptor plays a role in the initiation of endogenous cellular events associated with CNS injury.

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Section: Discussionmentioning

confidence: 99%