Dept. of Psychiatry,
University of Illinois at
Chicago & Jesse Brown VA
1601 West Taylor Street(m/c 912),
Chicago, IL 60612
Office Phone: 312-413-1310
Office Phone: 312-355-2614
Pandey SC, Sakharkar AJ, Tang L, Zhang H (2015) Potential role of adolescent alcohol exposure-induced amygdaloid histone modifications in anxiety and alcohol intake during adulthood. Neurobiology of Disease, March 23 (Epub ahead of print) PMID:25814047
Sakharkar AJ, Tang L, Zhang H, Chen Y, Grayson DR, Pandey SC (2014). Effects of acute ethanol exposure on anxiety measures and epigenetic modifiers in the extended amygdala of adolescent rats. Int J Neuropsychopharmacol. 17: 2057-2067 PMID: 24968059
Sakharkar AJ, Zhang H, Tang L, Baxstrom K, Shi G, Moonat S, Pandey SC (2014) Effects of histone deacetylase inhibitors on amygdaloid histone acetylation and neuropeptide Y expression: A role in anxiety-like and alcohol-drinking behaviors. Int. J Neuropsychopharmacol 17:1207-1220 PMID: 24528596
You C, Zhang H, Sakharkar AJ, Teppen TL, Pandey SC (2014) Reversal of deficits in dendritic spines, BDNF, and Arc expression in the amygdala during alcohol dependence by HDAC inhibitor treatment. Int. J Neuropsychopharmacol 17:313-322 PMID: 24103311
Moonat S, Sakharkar AJ, Zhang H, Tang L, Pandey SC (2013) Aberrant HDAC2-mediated histone modifications and synaptic plasticity in the amygdala predisposes to anxiety and alcoholism. Biol Psychiatry 73: 763-773 PMID: 23485013
Arora DS, Nimitvilai S, Teppen TL, McElvain MA, Sakharkar AJ,You C, Pandey SC, Brodie MS (2013) Hyposensitivity to gamma-aminobutyric acid in the ventral tegmental area during alcohol withdrawal: reversal by histone deacetylase inhibitors. Neuropsychopharmacol 38: 1674-1684 PMID: 23474591
Sakharkar AJ, Zhang H, Tang L, Shi G, Pandey SC (2012) Histone deacetylases(HDAC)- induced histone modifications in the amygdala: a role in rapid tolerance to the anxiolytic effects of ethanol. Alcohol Clin Exp Res. 36:61-71 PMID: 21790673
Moonat S, Sakharkar AJ, Zhang H, Pandey SC (2011) The role of amygdaloid brain-derived neurotrophic factor, activity-regulated cytoskeleton-associated protein and dendritic spines in anxiety and alcoholism. Addiction Biology 16:238-250 PMID: 21182574
Pandey SC, Ugale R, Zhang H, Tang L, Prakash A (2008) Brain chromatin remodeling: a novel mechanism of alcoholism. J Neurosci 28: 3729-3737.
Pandey SC, Zhang H, Roy A, Xu T (2005) Deficits in amygdaloid cAMP-responsive element-binding protein signaling play a role in genetic predisposition to anxiety and alcoholism. J Clin Investigation 115:2762-2773.
Pandey SC, Roy A, Zhang H (2004) Partial deletion of the CREB gene promotes alcohol-drinking behaviors. J Neuroscience 24:5022-5030.
Pandey SC (2003) Anxiety and alcohol abuse disorders: a common role for CREB and its target, the neuropeptide Y gene. Trends Pharmacological Sciences 24:456-460.
Pandey SC, Roy A, Zhang H (2003) The decreased phosphorylation of cyclic adenosine monophosphate (cAMP) response element binding (CREB) protein in the central amygdala acts as a molecular substrate for anxiety related to ethanol withdrawal in rats. Alcohol: Clin Exp Res 27:396-409.
Subhash C. Pandey, PhD
Director, Center for Alcohol Research in Epigenetics
Professor of biochemistry in Psychiatry
Professor of Anatomy and Cell Biology
Director, Neuroscience Alcoholism Research
Senior VA Career Research Scientist
Dr. Subhash Pandey is a nationally and internationally well-known neuroscientist in the alcohol addiction field and has contributed significantly towards a better understanding of the neurobiology of alcoholism. Two striking features of alcohol addiction are the rapid onset of tolerance to the acute effects of alcohol and the development of ethanol withdrawal symptoms after cessation of protracted ethanol consumption. Predisposition to alcohol abuse may involve abnormalities in the signaling cascade pathways that ultimately lead to abnormal gene transcription patterns in the specific neural circuitry of the brain. The long-term goal of Dr. Pandey’s alcohol research program is to elucidate the molecular and cellular mechanisms (cAMP responsive element binding protein (CREB) gene transcription factor and CREB-related genes; epigenetics) involved in anxiety, alcohol dependence and/or alcohol drinking behaviors so as to eventually provide a basis for designing drugs to treat alcohol abuse and anxiety disorders. Changes in CREB function may also lead to changes in synaptic structures, such as dendritic spines in the brain, during ethanol exposure and its withdrawal. Dr. Pandey’s lab has also involved in investigating the epigenetic mechanisms (chromatin remodeling due to histone modifications and DNA methylation) of anxiety and alcohol addiction. An additional area of Dr. Pandey’s interest is to identify the molecular and epigenetic mechanisms of adolescent alcohol exposure-induced psychopathology in adulthood. Some of his work has been highlighted by National Institutes of Health:
Molecular and cellular neurobiology of alcohol abuse and alcoholism.
- Epigenetic mechanisms of alcoholism and anxiety
- Neuronal signaling in alcoholism
- Role of CREB and related genes in alcoholism and anxiety
- Genetic basis of alcoholism
- Role of adolescent ethanol exposure on epigenetic and behavioral changes at adulthood
- Role of CB1 receptors in alcohol drinking behaviors