Expression of estrogen receptor alpha and beta in reactive astrocytes at the male rat hippocampus after status epilepticus.
Neuropathology
; 29(1): 55-62, 2009 Feb.
Article
em En
| MEDLINE
| ID: mdl-18627487
ABSTRACT
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)alpha and beta 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-ERalpha antibodies (MC-20 and PA1-309) and anti-ERbeta antibodies (PA1-310B and PA1-311). In control rats, both ERalpha and beta were expressed in the pyramidal cells predominantly at CA1 and CA3. ERalpha was expressed in the cytoplasm and the nucleus, whereas ERbeta was expressed in the cytoplasm of the pyramidal cells. After SE, according to the pyramidal cell loss at CA1, the number of ERalpha- and beta-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 ERalpha and beta under normal circumstances in adult male rats, whereas the targets of estrogen shift to the reactive astrocytes through ERalpha and beta after SE.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Estado Epiléptico
/
Astrócitos
/
Receptor alfa de Estrogênio
/
Receptor beta de Estrogênio
/
Hipocampo
Limite:
Animals
Idioma:
En
Revista:
Neuropathology
Assunto da revista:
NEUROLOGIA
/
PATOLOGIA
Ano de publicação:
2009
Tipo de documento:
Article
País de afiliação:
Japão