The ischemic damage in the hippocampal CA1 region following transient forebrain
ischemia, delayed neuronal death, is a typical apoptotic response, but the underlying mechanisms are not fully understood. We have reported that mild
hyperthermia (38 °C) accelerates DNA fragmentation of the gerbil CA1 pyramidal neurons following transient forebrain
ischemia. Recently, we reported that
galectin-3, a β-
galactosidase-binding
lectin, is spatio-temporally expressed only by activated microglial cells located within CA1 region following transient forebrain
ischemia in gerbils. Furthermore, expression of
galectin-3 and Iba-1 (a specific microglial cell marker) are strongly reduced by
hypothermia during ischemic insult. To further elucidate the effect of
hyperthermia on the expression of
galectin-3 by micloglia in delayed neuronal death, we examined immunohistochemical expression of
galectin-3 and Iba-1, in situ terminal dUTP-
biotin nick end labeling of DNA fragmentation (for determination of cell death) and
hematoxylin and
eosin staining (for morphological observation). We observed that between 37 °C and 39 °C, there was a temperature-dependent enhancement of
galectin-3 expression in microglial cells in the CA1 region following transient
ischemia. Apoptotic DNA fragmentation, detected by TUNEL staining, was observed in CA1 region in normothermia. This TUNEL staining was enhanced by
hyperthermia at 37.5 °C and 38 °C, but not at 39 °C.
Ischemia-induced neuronal degeneration in CA1 region in gerbil hippocampus subjected to
hyperthermia (37.5 °C, 38 °C and 39 °C) observed by HE staining is similar to that in normothermic gerbils. These findings imply that
galectin-3 expression in microglia may influence the survival of CA1 pyramidal neurons in cases such as
hyperthermia-related neuronal injury.