Rene Anand, Ph.D.

Associate Professor
Department of Pharmacology
796 Biomedical Research Towers
460 W. 12th Avenue
Columbus, OH  43210
Phone: (614) 292-1380
Fax: (614) 292-7232
E-mail: anand.20@osu.edu

Education
B.S.   - University of Madras (Loyola College), India
M.S.  - Indian Institute of Technology, Madras, India
Ph.D. - The Ohio State University, Columbus, OH

Postdoctoral Training
Salk Institute, San Diego, CA
University of Pennsylvania, Philadelphia, PA


Curriculum vitae


Research Interests

My laboratory is interested in understanding how addictive drugs progessively alter the molecular and cellular make up of specific neural circuits to sustain the development of compulsive addictive behavior.  We are focused on the actions of nicotine as a model for understanding mechanisms underlying CNS plasticity and for understainding mechanisms that serendipitously enhance the ability of the CNS to withstand neurotoxic insults characteristic of neurodegenerative diseases.

Nicotinic acetylcholine receptors (AChRs) are the primary mediators of the actions of nicotine in tobacco in the CNS.  Neuronal AChRs are ion channels assembled from multiple alpha and beta subunits that are associate with distinct sets of cytosolic proteins of different functions, only a few of which have been identified to date.  Some of these cytosolic proteins transiently associate with AChRs and regulate their assembly, trafficking, and turnover, whilst others cluster AChRs at membrane microdomains and/or serve as scaffolds for the assembly of signaling complexes that couple channel activity to specific intracellular signaling cascades.

Because the changes in the properties of neural circuits supporting addictive behavior, much like those underlying memory and learning, are initiated by dynamic and highly orchestrated changes in the density, functional organization, and properties of channels and receptors, it is likely that AChR associated cytsolic proteins, and the processes they regulate, participate in effecting these changes following repetitive activation of AChRs by nicotine.  These changes in AChRs then lead to downstream adaptive changes in neural networks within which they are expressed to change their emergent functional properties.  My laboratory has identified proteins involved in regulating AChR assembly, trafficking, turnover, synaptic targeting and signaling.  We are also studying the roles of these proteins in mediating AChR dysfunctions in animal models of schizophrenia, nicotine dependence, autism and Parkinson's disease.

Publications

Ruskin DN, Anand R, LaHoste GJ.  Chronic menthol attenuates the effects of nicotine in adolescent but not adult rats.  Nicotine & Tobacco Res (in press).

Ruskin DN, Anand R, LaHoste GJ. Menthol and nicotine oppositely modulate body temperature in the rat.  Eur J Pharmacol 559:161-164, 2007.

Brackmann M, Schuchmann S, Anand R, Braunewell KH. Neuronal Ca⁺⁺ sensor protein VILIP-1 affects cGMP signalling by regulating receptor recycling of guanylyl cyclase B in hippocampal neurons.  J Cell Science 118:24895-2505, 2005.

Ren XQ, Cheng SB, Treuil MW, Mukherjee J, Rao J, Lindstrom JM, Anand R.  Structural determinants of alpha4beta2 nicotinic acetylcholine receptor trafficking.  J Neurosci 25:6676-6686, 2005.

Lin L, Jeanclos EM, Braunewell KH, Gundelfinger ED, Anand R. Functional analysis of calcium-binding EF-hand of Visinin-like protein-1.  Biochem Biophy Res Comm 296:827-832, 2002.

Lin L, Jeanclos EM, Magdalen T, Braunewell KH, Gundelfinger ED, Anand R.  The calcium sensor proteing VILIP-1 modulates the surface expression and agonist-sensitivity of the nicotinic alpha4beta2 acetylcholine receptor.  J Biol Chem 277:41872-41878, 2002.