HDAC2 in Primary Sensory Neurons Constitutively Restrains Chronic Pain by Repressing α2δ-1 Expression and Associated NMDA Receptor Activity

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¹Center for Neuroscience and Pain Research, Department of Anesthesiology and Perioperative Medicine, University of Texas MD Anderson Cancer Center, Houston, Texas 77030
²Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, Texas 77030

Author contributions: H.-L.P. designed research; J.Z., S.-R.C., M.-H.Z., D.J., H.C., and L.W. performed research; R.A.D. contributed unpublished reagents/analytic tools; J.Z., S.-R.C., M.-H.Z., D.J., H.C., L.W., and H.-L.P. analyzed data; J.Z., S.-R.C., and H.-L.P. wrote the paper.
*J.Z. and S.-R.C. contributed equally to this work.

This work was supported by National Institutes of Health–National Institute of Neurological Disorders and Stroke Grant NS101880 and the N.G. and Helen T. Hawkins Endowment. We thank Sarah Bronson at MD Anderson Cancer Center for proofreading the manuscript.
The authors are employees of the University of Texas System, which currently holds a patent for targeting α2δ-1–bound glutamate receptors for treating diseases and disorders.
Correspondence should be addressed to Hui-Lin Pan at huilinpan{at}mdanderson.org

HHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS)
NS101880

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