C. Kaur et al., THE RESPONSE OF NEURONS AND MICROGLIA TO BLAST INJURY IN THE RAT-BRAIN, Neuropathology and applied neurobiology, 21(5), 1995, pp. 369-377
Rats subjected to a single non-penetrative blast were examined for pos
sible neuronal damage and glial reaction by immunohistochemistry and e
lectron 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 hypertrop
hied and their surface antigens, like complement type three receptors
(CR3), were upregulated. The blast wave also induced the vigorous expr
ession of major histocompatibility complex (MHC) class I and II (Ia) a
ntigens. In rats killed 21 days after the blast, the elevated immunore
activity of microglia had subsided and at 28 days both the microglial
external morphology and immunoreactivity were comparable to those of n
ormal animals. In rats killed 4-7 days after the blast, the neurons in
the cerebral and cerebellar cortex appeared normal except for the occ
urrence of some 'darkened' dendrites. The incidence of 'darkened' dend
rites 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-penet
rative blast in rats provokes a widespread microglial activation sugge
sting increased endocytosis and immunological responses. However, it r
emains uncertain whether such a drastic response was a direct activati
on of the cells by the blast wave or elicited indirectly by some chemi
cal factors released from the damaged brain tissues.