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Concurrent loss and proliferation of astrocytes following lateral fluid percussion brain injury in the adult rat
Author(s) -
HillFelberg Sandra J.,
McIntosh Tracy K.,
Oliver Douglas L.,
Raghupathi Ramesh,
Barbarese Elisa
Publication year - 1999
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19990715)57:2<271::aid-jnr13>3.0.co;2-z
Subject(s) - astrocyte , immunolabeling , hippocampal formation , hippocampus , proliferating cell nuclear antigen , immunohistochemistry , traumatic brain injury , pathology , medicine , population , glial fibrillary acidic protein , biology , anesthesia , central nervous system , environmental health , psychiatry
Astrocyte populations were analyzed over a period of 1 month in the hippocampus following lateral fluid percussion (FP) brain injury. Rats (n = 23) were subjected either to a brain injury of moderate severity, or to anesthesia and surgery without injury (n = 7). At 3 days, 1, 2, or 4 weeks postinjury, subgroups of animals were sacrificed and the brains removed and sectioned for histochemical analysis. The density of astrocytes, identified with gold sublimate staining, decreased significantly in the ipsilateral hippocampus of injured rats 3 days following injury, eventually falling to 64% of the total astrocyte population present in uninjured animals by 1 week postinjury. One month postinjury, the density of hippocampal astrocytes had returned to 85% of the total number of astrocytes observed in the hippocampus of uninjured animals. In order to characterize the post‐traumatic formation of new astrocytes, immunohistochemistry was performed using antibodies to proliferating cell nuclear antigen (PCNA) and to glial fibriallary acidic protein (GFAP). Positive immunolabeling for both PCNA and GFAP was most abundant at 3 days following FP brain injury in regions where the blood brain barrier was compromised, and was not detectable by 1 month postinjury. These results indicate that astrocyte proliferation after injury may be evoked by mitogens released from vascular sources, and may be an attempt to compensate for some of the astrocytic cell loss observed after injury. J. Neurosci. Res. 57:271–279, 1999. © 1999 Wiley‐Liss, Inc.