S. Kelly et al., Minimal ischaemic neuronal damage and HSP70 expression in MF1 strain mice following bilateral common carotid artery occlusion, BRAIN RES, 914(1-2), 2001, pp. 185-195
Investigation into the influence of specific genes and gene products upon t
he pathophysiology of cerebral ischaemia has been greatly enhanced by the u
se of genetically modified mice. A simple model of global cerebral ischaemi
a in mouse is bilateral common carotid artery occlusion (BCCAo) and the neu
ropathological impact of BCCAo has been investigated in several mouse strai
ns. Bilateral carotid occlusion produces extensive neuronal damage in C57BI
/6J strain mice and this damage is linked to posterior communicating artery
(PcomA) hypoplasticity in the circle of Willis. In the present study, we i
nvestigated the effect of BCCAo in MFI strain mice and compared them with C
57B1/6J mice. The neuropathological consequences of BCCAo were assessed usi
ng standard histochemical staining and heat shock protein 70 (HSP70) immuno
histochemical staining (to demarcate cells that had been ischaemically stre
ssed). The effect of BCCAo on mean arterial blood pressure (MABP) was also
measured. The plasticity of the circle of Willis was recorded using carbon
black perfusion. MF1 mice displayed significantly less ischaemic neuronal d
amage and HSP70 immunoreactivity compared to C57B1/6J mice following 10-20
min BCCAo. Moreover, ischaemic neuronal damage and HSP70 immunoreactivity i
n MF1 mice subjected to extended BCCAo (25-45 min) was never as extensive o
r widespread as that observed in C57BI/6J mice after 20 min BCCAo. MABP in
MF1 mice (102 +/-5 mmHg) was significantly higher than in C57BI/6J mice (87
+/-5) during 20 min BCCAo. MABP in MF1 mice during 20 and 40 min (103 +/-
12 mmHg) BCCAo remained above pre-occlusion values for the entire occlusion
period. MF1 mice had significantly greater circle of Willis plasticity (mo
re PcomAs) than C57BI/6J mice did. These data indicate that MFI mice are le
ss susceptible to BCCAo than C57BI/6J mice and that this could be due to ma
intained increases in MABP during BCCAo and the lower prevalence of abnorma
lities of the circle of Willis in MFI mice. (C) 2001 Elsevier Science BY. A
ll rights reserved.