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The response of neurons and microglia to blast injury in the rat brain
Author(s) -
Kaur C.,
Singh J.,
Lim M. K.,
Ng B. L.,
Yap E. P. H.,
Ling E. A.
Publication year - 1995
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1995.tb01073.x
Subject(s) - microglia , major histocompatibility complex , immunohistochemistry , pathology , biology , precursor cell , antigen , immunology , neuroscience , medicine , inflammation , cell , genetics
Rats subjected to a single non‐penetrative blast were examined for possible neuronal damage and glial reaction by immunohistochemistry and electron microscopy. The most dramatic feature in rats killed between 1 and 14 days after the blast was the widespread response of microglial cells in various parts of the brain in which the cells were hypertrophied and their surface antigens, like complement type three receptors (CR3), were upregulated. The blast wave also induced the vigorous expression of major histocompatibility complex (MHC) class I and II (Ia) antigens. In rats killed 21 days after the blast, the elevated immunoreactivity of microglia had subsided and at 28 days both the microglial external morphology and immunoreactivity were comparable to those of normal animals. In rats killed 4–7 days after the blast, the neurons in the cerebral and cerebellar cortex appeared normal except for the occurrence of some ‘darkened dendrites’. The incidence of ‘darkened’ den‐drites was most common in rats killed at day 14 but they were absent at 21 and 28 days. Microglial cells were closely associated with some of the ‘darkened’ dendrites. Results in this study show that a non‐penetrative blast in rats provokes a widespread microglial activation suggesting increased endocytosis and immunological responses. However, it remains uncertain whether such a drastic response was a direct activation of the cells by the blast wave or elicited indirectly by some chemical factors released from the damaged brain tissues.