PMID- 23216580 OWN - NLM STAT- MEDLINE DCOM- 20130204 LR - 20211021 IS - 1528-1167 (Electronic) IS - 0013-9580 (Print) IS - 0013-9580 (Linking) VI - 53 Suppl 9 IP - 0 9 DP - 2012 Dec TI - Molecular pathways controlling inhibitory receptor expression. PG - 71-8 LID - 10.1111/epi.12036 [doi] AB - Epilepsy is a disease of complex etiology, and multiple molecular mechanisms contribute to its development. Temporal lobe epilepsy (TLE) may result from an initial precipitating event such as hypoxia, head injury, or prolonged seizure (i.e., status epilepticus [SE]), that is followed by a latent period of months to years before spontaneous seizures occur. gamma-Aminobutyric acid (GABA)(A) receptor (GABA(A) R) subunit changes occur during this latent period and may persist following the onset of spontaneous seizures. Research into the molecular mechanisms regulating these changes and potential targets for intervention to reverse GABA(A) R subunit alterations have uncovered seizure-induced pathways that contribute to epileptogenesis. Several growth or transcription factors are known to be activated by SE, including (but not limited to): brain-derived neurotrophic factor (BDNF), cAMP response element binding protein (CREB), inducible cAMP early repressor (ICER), and early growth response factors (Egrs). Results of multiple studies suggest that these factors transcriptionally regulate GABA(A) R subunit gene expression in a way that is pertinent to the development of epilepsy. This article focuses on these signaling elements and describes their possible roles in gene regulatory pathways that may be critical in the development of chronic epilepsy. CI - Wiley Periodicals, Inc. (c) 2012 International League Against Epilepsy. FAU - Grabenstatter, Heidi L AU - Grabenstatter HL AD - Translational Epilepsy Program, University of Colorado School of Medicine, Aurora, Colorado 80045, USA. FAU - Russek, Shelley J AU - Russek SJ FAU - Brooks-Kayal, Amy R AU - Brooks-Kayal AR LA - eng GR - F31 NS051943/NS/NINDS NIH HHS/United States GR - F31NS065629/NS/NINDS NIH HHS/United States GR - R01NS051710/NS/NINDS NIH HHS/United States GR - R01 NS051710/NS/NINDS NIH HHS/United States GR - F31 NS065629/NS/NINDS NIH HHS/United States GR - F31NS051943/NS/NINDS NIH HHS/United States GR - R01 NS050393/NS/NINDS NIH HHS/United States GR - R01NS050393/NS/NINDS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Review PL - United States TA - Epilepsia JT - Epilepsia JID - 2983306R RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Cyclic AMP Response Element-Binding Protein) RN - 0 (Early Growth Response Transcription Factors) RN - 0 (Nerve Growth Factors) RN - 0 (Neurotransmitter Agents) RN - 0 (Receptors, GABA-A) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/metabolism MH - Cyclic AMP Response Element-Binding Protein/metabolism MH - Early Growth Response Transcription Factors/metabolism MH - Epilepsy/*metabolism/physiopathology MH - Epilepsy, Temporal Lobe/metabolism MH - Humans MH - *Metabolic Networks and Pathways/drug effects MH - Nerve Growth Factors/metabolism MH - Neurotransmitter Agents/metabolism MH - Receptors, GABA-A/*biosynthesis/metabolism MH - *Signal Transduction/drug effects PMC - PMC3776022 MID - NIHMS411477 COIS- Disclosures: The authors have no conflicts of interest to disclose. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines. EDAT- 2012/12/19 06:00 MHDA- 2013/02/05 06:00 PMCR- 2013/12/01 CRDT- 2012/12/11 06:00 PHST- 2012/12/11 06:00 [entrez] PHST- 2012/12/19 06:00 [pubmed] PHST- 2013/02/05 06:00 [medline] PHST- 2013/12/01 00:00 [pmc-release] AID - 10.1111/epi.12036 [doi] PST - ppublish SO - Epilepsia. 2012 Dec;53 Suppl 9(0 9):71-8. doi: 10.1111/epi.12036.