Effects of Transient Forebrain Ischemia on the Hippocampus of the Mongolian Gerbil (Meriones unguiculatus): An Immunohistochemical Study

Abstract

In the Mongolian gerbil, bilateral common carotid artery occlusion (BCCAO) for several minutes induces ischemia and delayed neuronal cell death in the CA1 region of the hippocampus due to their incomplete Circle of Willis. In the present study, the expression of fibroblast growth factor 2 (FGF2), its receptors (FGFR1 and FGFR2), glial fibrillary acidic protein (GFAP), and isolectin B4 (ISLB4) was investigated by immunohistochemical and lectin-binding methods after BCCAO was performed for 5 min in gerbils. One day after BCCAO, the pyramidal cells of the CA1 region of the hippocampus showed degenerative changes and lowered expression of FGF2, FGFR1, and FGFR2. Three days after BCCAO, there was an increase in GFAP-positive astrocytes and ISLB4-positive microglial cells. From five to 10 days after BCCAO, intense neuronal cell death in the stria pyramidale of the hippocampal CA1 region was observed, as well as an increase in GFAP-positive astrocytes and decrease in ISLB4-positive microglial cells. These results indicate that transient forebrain ischemia induces neuronal cell death with lowered expression of FGF2 and its receptors, and that the activation of glial cells may not directly lead to neuronal cell death.

CHIP ameliorates neuronal damage in H2O2-induced oxidative stress in HT22 cells and gerbil ischemia

“…In this study, we visualized astrocytes and microglia in the hippocampal CA1 region 4 days after ischemia induction. Ischemic insults cause morphological changes in astrocytes and microglia and aggregation of microglia in damaged regions [49][50][51] . Treatment with Tat-CHIP, but not Con-CHIP, decreased the activation of astrocytes and microglia in a concentrationdependent manner.…”

Long‐term fate of grafted hippocampal neural progenitor cells following ischemic injury

“…This model allows researchers to mimic an ischemia‐induced CA1 hippocampal cell death in a reproducible manner (Pulsinelli et al, ; Kirino and Sano, ). After induction of global ischemia, microglia and astrocytes are gradually activated and numerous inflammatory cytokines are released from glial cells (Yan et al, ,b; Okada et al, ). It has been previously shown that in astrocytes activated in response to ischemic brain injury, the nestin reexpression plays a role in transformation of normal astrocytes to reactive ones (Cho et al, ).…”

Transient forebrain ischemia induces impairment in cognitive performance prior to extensive neuronal cell death in Mongolian gerbil (Meriones unguiculatus)

“…Some gerbils exhibit seizure-like convulsions; however, the present study was carried out without considering the occurrence of such convulsions, as it has been reported by Herrmann et al [ 12 ] that these inherent epileptic seizures do not influence the outcome of brain injury after ischemia, making the gerbils a reliable model for studies on transient brain ischemia. BCCAO was performed as previously described [ 27 ]. Briefly, the animals were anesthetized with isoflurane.…”

“…A transient episode of cerebral ischemia causes delayed neuronal death of Cornet d'Ammon 1 (CA1) pyramidal cells in the hippocampus, which takes 2–3 days to become morphologically obvious [ 18 19 ], and delayed neuronal cell death in the hippocampal CA1 region at 4 to 7 days after an ischemic insult [ 15 26 ]. In our previous study, we reported that CA1 pyramidal cells with pale cytoplasm are observed 1 day after BCCAO, and that atrophy of those pyramidal cells is first observed 3 days post-operation; moreover, it worsens over time [ 27 ]. In rats, there is a correlation between hippocampal damage and a deficit in spatial learning following global cerebral ischemia [ 6 ].…”