Title

Neuronal and astrocytic apoptosis after subarachnoid hemorrhage: A possible cause for poor prognosis

Document Type

Article

Abstract

Clinical evidence suggests that factors other than cerebral vasospasm, such as delayed neuronal and astrocytic cell death, may play a role in the poor prognosis of patients with subarachnoid hemorrhage (SAH). Here we examined this using immunohistochemistry and confocal microscopy in 3 different brain areas in a dog model of SAH. Using antibodies against neuronal marker neuronal nuclear protein (NeuN) and astrocyte marker glial fibrillary acidic protein (GFAP) in conjunction with apoptosis marker (cleaved caspase-3), we quantified neurons and astrocytes to monitor the degree of apoptosis in both groups. Experimental SAH group showed 44 ± 1% caspase-3 positive neurons in comparison to the 2.0 ± 0.1% in the control group (P < 0.001, 6 animals each group). For astrocytes, a total 25 ± 1% were caspase-3 positive in day 7 SAH group, as compared to 0.40 ± 0.01% for controls (P < 0.001). Regional analysis revealed that neuronal caspase-3 immunoreactivity in all 3 regions were significantly higher (P < 0.001) in SAH animals than that in the control animals. However, the analysis of total area, size and signal co-localization of GFAP with caspase-3 indicated that astrocytic reactivity and proliferation are seen primarily in the hippocampal area, with the least changes detectable in the brainstem. We conclude that in the dog model, there was a significant increase of neuronal and astrocytic cleaved caspase-3, possibly reflecting apoptosis, following SAH induction. These changes coupled with neurological deterioration seen in patients may present a possible reason for the poor outcome in SAH patients. © 2008 Elsevier B.V. All rights reserved.

Publication Date

10-31-2008

Publication Title

Brain Research

ISSN

00068993

Volume

1238

First Page

163

Last Page

171

PubMed ID

18786513

Digital Object Identifier (DOI)

10.1016/j.brainres.2008.08.031

https://doi.org/10.1016/j.brainres.2008.08.031

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