Duke Institute for Brain Sciences

My lab studies the mechanisms and consequences of activity-regulated transcription in the nervous system. Neuronal activity leads to long-lasting changes in brain function in part through the regulated expression of new gene products that contribute to synaptic function and neuronal excitability. Part of the work in my lab is devoted to understanding how the activation of intracellular calcium signaling pathways activates or represses transcription factors in order to drive these changes in gene expression. We have been particularly interested in epigenetic mechanisms of transcriptional regulation, which include histone modifications and DNA methylation, as these processes have the potential to confer very long lasting changes upon the transcriptional potential of genes. Other projects in the lab address the neurobiological consequences of disrupting regulated transcription. Our recent studies have focused on the role of transcriptional regulatory pathways that mediate persistant neural adaptations to psychostimulant drugs of abuse.

Postdoctoral Fellow, Children's Hospital, Boston, Molecular Neurobiology, 1998-2005

M.D., Harvard Medical School, 1998

Ph.D., Harvard University, Neuroscience, 1998

B.A., Cornell University, 1989

Hutchinson, A.N., Deng, J.V., Cohen, S., and West, A.E. (2012) Phosphorylation of MeCP2 at Ser421 contributes to chronic antidepressant action. J Neurosci. 32:14355-14363. PMCID: PMC3480513.

Lyons, M.R., Schwarz, C.S., and West A.E. (2012) Members of the MEF2 transcription factor family differentially regulate Bdnf transcription in response to neuronal depolarization. J Neurosci. 32:12780-12785. PMCID: PMC3487695.

Deng, J.V., Rodriguez, R.M., Hutchinson, A.N., Kim, I.-H., Wetsel, W.C., and West, A.E. (2010) MeCP2 in the nucleus accumbens contributes to neural and behavioral responses to psychostimulants. Nat Neurosci. 13: 1128-1136. PMCID: PMC2928851.