My research is generally concerned with understanding how the neurotransmitters of the basal ganglia contribute to the generation of appetitive behaviors. I am particularly interested in the impact of the ascending mesencephalic dopamine systems. These groups of neurons, while relatively small, project to a large number of forebrain sites and are known to profoundly influence motor and affective behaviors. We are interested in determining how these systems interact with others to produce such effects and how these neurotransmitter interactions may be changed when an organism is exposed repeatedly to pharmacological and environmental stimuli. We and others have shown that exposing rats repeatedly to psychotropic drugs or environmental stressors leads to the induction and eventual expression of sensitization (reverse tolerance) in mesolimbic dopamine neurotransmission. 

Currently, our research is aimed, first, at determining how this sensitization is produced and, second, at understanding how such changes may influence the expression of various behaviors in the rat. In the first case, we are using a variety of behavioral, intracranial drug delivery, biochemical and neuropharmacological techniques to determine which aspects of dopamine neurotransmission become enhanced (transmitter release, receptor regulation and function) and to assess the contribution of other neurotransmitter projections and receptor fields (excitatory amino acids, ACh, GABA). In the second, we are investigating the relation between the expression of sensitization in the mesolimbic dopamine systems and an organism's predisposition to substance abuse. We are assessing the extent to which various manipulations, known to sensitize dopamine neuron reactivity, promote psychotropic drug seeking and self-administration in rats.

Suto, N., Austin, J.D. and Vezina, P. (2001)  Locomotor response to novelty predicts rats' propensity to self-administer nicotine. Psychopharmacology 158: 175-180.

Hu, X-T., Koeltzow, T.E., Cooper, D.C., Robertson, G.S., White, F.J. and Vezina, P. (2002)  Repeated ventral tegmental area amphetamine administration alters D₁ dopamine receptor signaling in the nucleus accumbens.  Synapse 45: 159-170.

Kim, J-H. and Vezina, P. (2002)  The mGlu2/3 receptor agonist LY379268 blocks the expression of locomotor sensitization by amphetamine. Pharmacol. Biochem. Behav. 73: 333-337. (invited)

Suto, N., Austin, J.D., Tanabe, L., Kramer, M., Wright, D. and Vezina, P. (2002) Previous exposure to VTA amphetamine enhances cocaine self-administration in a D₁ dopamine receptor dependent manner. Neuropsychopharmacology 27: 970-979.

Vezina, P., Lorrain, D.S., Arnold, G.M., Austin, J.D. and Suto, N. (2002)  Sensitization of midbrain dopmaine neuron reactivity promotes the pursuit of amphetamine. J. Neurosci. 22: 4654-4662.

Kim, J-H., Creekmore, E. and Vezina, P. (2003). Microinjection of CART peptide 55-102 into the nucleus accumbens blocks amphetamine-induced locomotion. Neuropeptides 37: 369-373.

Koeltzow, T.E., Austin, J.D. and Vezina, P. (2003) Behavioral sensitization to quinpirole is not associated with increased nucleus accumbens dopmaine overflow. Neuropharmacology 44: 102-110. (Neuroscion highlight)

Suto N., Tanabe, L.M., Austin J.D., Creekmore E. and Vezina, P. (2003)  Previous exposure to VTA amphetamine enhances cocaine self-administration in an NMDA. AMPA/kainite and metobotropic glutamate receptor dependent manner. Neuropsychopharmacology 28: 629-639.

Vezina, P. and  Suto, N. (2003) Glutamate and the self-administration of psychomotor stimulant drugs.  In B.H. Herman (Ed), Glutamate and Addiction, pp. 183-200. Totwa, NJ: Humana Press. (invited)

Vezina, P. (2004) Sensitization of midbrain dopamine neuron reactivity and the self-administration of psychomotor stimulant drugs. Neurosci. Biobehav. Rev. 27: 827-839. (invited)