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Expression of estrogen receptor α and β in reactive astrocytes at the male rat hippocampus after status epilepticus
Author(s) -
Sakuma Satoru,
Tokuhara Daisuke,
Hattori Hideji,
Matsuoka Osamu,
Yamano Tsunekazu
Publication year - 2009
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/j.1440-1789.2008.00946.x
Subject(s) - hippocampal formation , estrogen , estrogen receptor , status epilepticus , endocrinology , hippocampus , medicine , neuroprotection , gliosis , astrocyte , biology , chemistry , central nervous system , neuroscience , epilepsy , cancer , breast cancer
Estrogen is neuroprotective against status epilepticus (SE)‐induced hippocampal damage in female animals. In male animals, estrogen is converted from testosterone via aromatization the activity of which is upregulated by brain damage. However, it is controversial whether estrogen is neuroprotective or neuroinvasive against male hippocampal damage after SE. In order to understand the role of estrogen, it is important to elucidate the distribution manner of estrogen receptor (ER)α and β as the targets of estrogen. In this study, we examined the time course changes of ERs in adult male rat hippocampus after SE using anti‐ERα antibodies (MC‐20 and PA1‐309) and anti‐ERβ antibodies (PA1‐310B and PA1‐311). In control rats, both ERα and β were expressed in the pyramidal cells predominantly at CA1 and CA3. ERα was expressed in the cytoplasm and the nucleus, whereas ERβ was expressed in the cytoplasm of the pyramidal cells. After SE, according to the pyramidal cell loss at CA1, the number of ERα‐ and β‐immunoreactive pyramidal cells decreased up to day 21. On the other hand, reactive astrocytes, which newly appeared after SE and formed gliosis at CA1, were confirmed to express both ERs in the nucleus, cytoplasm, and process. There were no differences in immunoreactivity between antibodies. Our results indicate that endogenous estrogen affects the pyramidal cells through ERα and β under normal circumstances in adult male rats, whereas the targets of estrogen shift to the reactive astrocytes through ERα and β after SE.