17β-estradiol attenuates injury-induced microglia activation in the oculomotor nucleus
| Autor: | Árpád Párducz, László Siklós, Eszter Csakvari, Andrea Gyenes, Zsófia Hoyk |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Nervous system
medicine.medical_treatment Central nervous system Biology Neuroprotection Oculomotor nucleus Mice Oculomotor Nerve Oculomotor Nerve Diseases medicine Animals Gliosis Mice Inbred BALB C Estradiol Microglia General Neuroscience Nerve injury Disease Models Animal Neuroprotective Agents medicine.anatomical_structure Neuroglia Female Axotomy medicine.symptom Neuroscience |
| Zdroj: | Neuroscience. 171:677-682 |
| ISSN: | 0306-4522 |
| Popis: | Recent studies provide increasing data indicating the prominent role of estrogens in protecting the nervous system against the noxious consequences of nerve injury. It is also clear that in the process of nerve injury and recovery not only the neurons, but the glial cells are also involved and they are important components of the protective mechanisms. In the present article the effect of 17β-estradiol on injury-induced microglia activation was studied in an animal model. Peripheral axotomy of the oculomotor neurons was achieved by the removal of the right eyeball including the extraocular muscles of ovariectomized adult mice. The time course and the extent of microglia activation was followed by the unbiased morphometric analysis of CD11b immunoreactive structures within the oculomotor nucleus. The first sign of microglia activation appeared after 24 h following injury, the maximal effect was found on the fourth day. In ovariectomized females hormone treatment (daily injection of 17β-estradiol, 5 μg/100 g b.w.) decreased significantly the microglia reaction at postoperative day 4. Our results show that microglia response to nerve injury is affected by estradiol, that is these cells may mediate some of the hormonal effects and may contribute to protective mechanisms resulting in the structural and functional recovery of the nervous system. |
| Databáze: | OpenAIRE |
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