pavel ortinski

Pavel I. Ortinski, Ph.D.        
Assistant Professor
Training:
Postdoctoral: The Children’s Hospital
of Philadelphia, University of
Pennsylvania
Ph.D.: Georgetown University
Contact Information:
Phone: 803 216 3528
Fax: 803 216 3538
E-mail: pavel.ortinski@uscmed.sc.edu
Web Page

Research Focus:

Our laboratory investigates neuronal correlates of addictive behaviors. The main goal is to understand how exposure to drugs of abuse modifies neuronal transmission in brain areas critical for reward and motivation processing. Our most recent studies focused on glutamate receptor signaling in medium spiny neurons of the nucleus accumbens in rats self-administering cocaine. Among other interesting findings, we saw that activation of dopamine (D1) receptors in cocaine exposed rats can normalize AMPA receptor signaling by recruiting cannabinoid (CB1) receptors and that cocaine elicits an adaptive interaction between extrasynaptic NMDA receptors and glutamate re-uptake transporters. These observations draw attention to the complexity of cocaine effects on neuronal signaling, but they are only a fraction of neuroadaptations known to arise following cocaine exposure. Indeed, a major unanswered question is whether it is possible to isolate those neuronal changes responsible for the expression of a “hypermotivated” state that leads to pursuit of a drug reward. To examine this and similar questions, we use a variety of tools including: in vitro electrophysiology, behavioral pharmacology, molecular assays, electrochemical analyses, and imaging techniques.

lab image

Recent Publications:

PubMed Link:

  • Ortinski P.I., Vassoler F.M., Carlson G.C., and Pierce R.C.: Temporally dependent changes in cocaine-induced synaptic plasticity in the nucleus accumbens shell are reversed by D1-like dopamine receptor stimulation. Neuropsychopharmacology, 2012, 37:1671-82.
  • Gandal, M.J., Sisti, J., Klook, K., Ortinski, P.I.,  Leitman, V., Liang, Y., Thieu, T., Pierce, R.C., Jonak, G., Gur R.E., Carlson, G., Siegel, S.J.: GABA(B)-mediated rescue of altered excitatory-inhibitory balance, gamma synchrony and behavioral deficits following constitutive NMDAR-hypofunction. Translational Psychiatry, 2012, 2, e142, doi:10.1038/tp.2012.69.
  • Ortinski, P.I., Turner, JR., Pierce R.C. Extrasynaptic targeting of NMDA receptors following D1 dopamine receptor activation and cocaine self-administration. Journal of Neuroscience, 2013, 33:9451-61.
  • Mietlicki-Baase, E.G., Ortinski, P.I., Rupprecht, L.E., Olivos, D.R., Alhadeff, A.L., Pierce, R.C., Hayes, M. The food intake-suppressive effects of glucagon-like peptide-1 receptor signaling in the ventral tegmental area are mediated by AMPA/kainate receptors. Am J Physiol Endocrinol Metab, 2013, 305:E1367-74.
  • Briand, L.A., Kimmey, B.A., Ortinski, P.I., Huganir, R.L., Pierce, R.C. Disruption of Glutamate Receptor-Interacting Protein in nucleus accumbens enhances vulnerability to cocaine relapse. Neuropsychopharmacology, 2014, 39:759-69.
  • Ortinski, P.I: Cocaine-induced changes in NMDA receptor signaling. Mol Neurobiology, 2014, doi: 10.1007/s12035-014-8636-6.