| Autor: |
Grabenstatter, Heidi L, Cogswell, Meaghan, Cruz Del Angel, Yasmin, Carlsen, Jessica, Gonzalez, Marco I., Raol, Yogendra H., Russek, Shelley J., Brooks-Kayal, Amy R. |
| Předmět: |
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| Zdroj: |
Epilepsia (Series 4); Nov2014, Vol. 55 Issue 11, p1826-1833, 8p |
| Abstrakt: |
Objective Temporal lobe epilepsy ( TLE) is frequently medically intractable and often progressive. Compromised inhibitory neurotransmission due to altered γ-aminobutyric acid ( GABA)A receptor α4 subunit ( GABAARα4) expression has been emphasized as a potential contributor to the initial development of epilepsy following a brain insult (primary epileptogenesis), but the regulation of GABAARα4 during chronic epilepsy, specifically, how expression is altered following spontaneous seizures, is less well understood. Methods Continuous video-electroencephalography ( EEG) recordings from rats with pilocarpine-induced TLE were used to capture epileptic animals within 3 h of a spontaneous seizure ( SS), or >24 h after the last SS, to determine whether recent occurrence of a seizure was associated with altered levels of GABAARα4 expression. We further evaluated whether this GABAARα4 plasticity is regulated by signaling mechanisms active in primary epileptogenesis, specifically, increases in brain-derived neurotrophic factor ( BDNF) and early growth response factor 3 (Egr3). Results Elevated levels of GABAARα4 messenger RNA (mRNA) and protein were observed following spontaneous seizures, and were associated with higher levels of BDNF and Egr3 mRNA. Significance These data suggest that spontaneous, recurrent seizures that define chronic epilepsy may influence changes in GABAARα4 expression, and that signaling pathways known to regulate GABAARα4 expression after status epilepticus may also be activated after spontaneous seizures in chronically epileptic animals. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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