BDNF Selectively Regulates GABAA Receptor Transcription by Activation of the JAK/STAT Pathway
Ingrid V. Lund,1* Yinghui Hu, YogendraSinh H. Raol,2 Rebecca S. Benham, Ramona Faris, Shelley J. Russek,4† Amy R. Brooks-Kayal
1Neuroscience Graduate Group and Departments of Neurology and Pediatrics, University of Pennsylvania, Philadelphia, PA 19104, USA.
2Division of Neurology, Children's Hospital, Philadelphia, PA 19104, USA.
3Program in Biomedical Neurosciences, Boston University School of Medicine, Boston, MA 02118, USA.
4Laboratory of Translational Epilepsy, Department of Pharmacology, Boston University School of Medicine, Boston, MA 02118, USA.
5Laboratory of Molecular Neurobiology, Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA 02118, USA.
6Division of Neurology, Department of Pediatrics, University of Colorado Denver School of Medicine, Denver, CO 80045, USA.
7Division of Neurology, The Children's Hospital, 13123 East 16th Avenue, B155, Aurora, CO 80045, USA.
*These authors contributed equally to this work.
This PDF file includes:
- Fig. S1. GABAR α1 mRNA expression is decreased in DG after pilocarpine-induced SE.
- Fig. S2. Mutant CRE site does not bind CREB or ICER after DNA pull down.
- Fig. S3. BDNF-induced ICER is not dependent on PKA, CaM kinase, or PI 3-kinase activation.
- Fig. S4. Inhibition of JAK/STAT pathway via slow infusion of P6 beginning 48 hours before SE does not affect SE.
- Fig. S5. No effect of P6 on PKA-induced ICER synthesis.
- Fig. S6. BDNF increases binding of pSTAT3 to the endogenous ICER promoter as compared to isotype antibody control.
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†To whom correspondence should be addressed. E-mail:(S.J.R.) and (A.R.B.)