Jose A. Moron-Concepcion, Ph.D.

Pain Center

Neurosciences Program
Molecular Cell Biology Program
Biochemistry, Biophysics, and Structural Biology Program

  • 314 362-0078

  • 5560 Clinical Sciences Research Building



  • opioids, addiction, pain, molecular mechanisms, animal models

  • Elucidating the molecular mechanisms underlying opiate dependence

Research Abstract:

Studies in our laboratory are focused in elucidating the molecular mechanisms underlying opiate dependence. In addition, given the fact that opiates are widely used in the clinic for the treatment of acute and chronic pain conditions, and the current rise in the rates of addiction to, and misuse of prescription opiates, we are interested in examining the effects of the presence of chronic pain on opiate intake and in the motivation for opiate self-administration. Additional studies will also be conducted in order to determine the effects of chronic pain on neural circuits within the reward pathway. Finally, it has been reported that opioid receptors (mu, delta, kappa) can form heterodimers following chronic opiate administration. The formation of these receptor heteromers has been reported to be involved in the mechanisms underlying opiate tolerance. Therefore, in an additional project we will examine whether the formation of a mu-delta opioid receptor heteromer is responsible for the expression of observed analgesic tolerance upon chronic opiate administration with the overall goal to develop novel drugs to enhance the analgesic properties of the opiate without side effects (i.e. tolerance).

Selected Publications:

Inflammatory pain promotes increased opioid self-administration: role of dysregulated ventral tegmental area mu opioid receptors
L. Hipolito, A. Wilson-Poe, Y. Campus-Jurado, E. Zhong, J. Gonzalez-Romero, L. Virag, R. Whittington, S. Comer, S. Carlton, B. Walker, M. Bruchas and J.A. Morón. Journal of Neuroscience 2015 Sept 2:35(35): 12217-12231

Does the kappa opioid receptor system contribute to pain aversion?
Cahill CM, Taylor AM, Cook C, Ong E, Morón JA, et al.
Frontiers in pharmacology. 2014; 5:253.

Hippocampal long-term potentiation is disrupted during expression and extinction but is restored after reinstatement of morphine place preference.
Portugal GS, Al-Hasani R, Fakira AK, Gonzalez-Romero JL, Melyan Z, et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 2014; 34(2):527-38.

Increased small conductance calcium-activated potassium type 2 channel-mediated negative feedback on N-methyl-D-aspartate receptors impairs synaptic plasticity following context-dependent sensitization to morphine.
Fakira AK, Portugal GS, Carusillo B, Melyan Z, Morón JA.
Biological psychiatry. 2014; 75(2):105-14. NIHMSID: NIHMS476702

Gp120 in the pathogenesis of human immunodeficiency virus-associated pain.
Yuan SB, Shi Y, Chen J, Zhou X, Li G, et al.
Annals of neurology. 2014; 75(6):837-50. NIHMSID: NIHMS575704

Implication of delta opioid receptor subtype 2 but not delta opioid receptor subtype 1 in the development of morphine analgesic tolerance in a rat model of chronic inflammatory pain.
Beaudry H, Gendron L, Morón JA.
The European journal of neuroscience. 2015; 41(7):901--7. NIHMSID: NIHMS649319

In vivo activation of the SK channel in the spinal cord reduces the NMDA receptor antagonist dose needed to produce antinociception in an inflammatory pain model.
Hipólito L, Fakira AK, Cabañero D, Blandón R, Carlton SM, et al.
Pain. 2015; 156(5):849-58. NIHMSID: NIHMS660860

Upregulation of dopamine D2 receptors in the nucleus accumbens indirect pathway increases locomotion but does not reduce alcohol consumption.
Gallo EF, Salling MC, Feng B, Morón JA, Harrison NL, et al.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2015; 40(7):1609-18.

Last Updated: 3/22/2017 2:20:42 PM

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