Dr. Peter Kalivas, PhD.

Professor and Chair of Neurosciences

Tel: (843) 792-4400
Fax: (843) 792-4423
Email: kalivasp@musc.edu

Education

BS, Biology, 1974, Western Washington University
PhD, Pharmacology, 1980, University of Washington, Seattle
Postdoctoral Fellowship, 1980-82, University of North Carolina

Research Interests

Neurobiology of drug addiction including neuroadaptions in molecular, neuronal and behavioral systems. Neural circuitry mediating the translation of motivation into adaptive behaviors.

Publications

McFarland K, CC Lapish and PW Kalivas. 2003. Glutamate, not dopamine, in the accumbens core mediates cocaine-induced reinstatement of drug-seeking behavior. J. Neuroscience, 23: 3531-3537

Xi, Z-X, S Ramamoorthy, H Shen, R Lake, DJ Samuvel and PW Kalivas. 2003. Neuroadaptations in GABA transmission in the nucleus accumbens following repeated cocaine. J.Neuroscience, 23: 3498-3505

Baker, DA, McFarland K, Lake RW, Shen H, Ghasemzadeh MB, Tang X, Toda S and PW Kalivas. 2003. Reduced extracellular glutamate and cystine-glutamate exchange underlie cocaine-seeking behavior Nat Neuroscience, 6: 743-749.

Toda, S, JF McGinty and PW Kalivas. 2002. Long-lasting alterations in gene expression in mesocorticolimbic circuitry after chronic cocaine administration: a DNA macroarray study. J.Neurochem, 82: 1290-1299

Baker, DA, Xi, Z-X, Shen, H, Swanson, CJ and PW Kalivas. 2002. The primary source and neuronal function of in vivo extracellular glutamate. J.Neuroscience, 22: 9134-9141

Current Lab Research

We are studying how the brain adapts to repeated exposure by drugs of abuse, with a focus on psychostimulants such as cocaine and amphetamine. These adaptations manifest themselves as classic symptoms of addiction, including drug craving and paranoia.

We study these adaptations first by defining the normal state of the brain circuitry involved using neurochemical, anatomical and behavioral techniques. This has led to the characterization of a circuit, termed the motive circuit (see below), that is intimately involved in translating motivational stimuli into normal adaptive behavioral responses. We then superimpose on this circuit repeated exposure to psychostimulants and examine changes in the function of the motive circuit using molecular, neurochemical and behavioral techniques.

This strategy has uncovered many novel neuroadaptions. Notably, the recruitment of glutamate transmission from the cortex in addiction behavior and alterations of gene expression, including novel genes such as NAC-1. The role of changes in gene expression in addiction is validated by microinjecting either antisense oligonucleotide or viral vectors into selected brain nuclei to under or over express, respectively, the gene of interest. Animals with altered expression are then examined in various behavioral models of addiction such as drug self-administration and reinstatement, and locomotor sensitization.

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