Genomes and Genes
Theodore J Price
Affiliation: University of Arizona
- AMPK: An emerging target for modification of injury-induced pain plasticityTheodore J Price
Department of Pharmacology, The University of Arizona School of Medicine, United States Bio5 Institute, The University of Arizona School of Medicine, United States Graduate Interdisciplinary Program in Neuroscience, The University of Arizona School of Medicine, United States Electronic address
Neurosci Lett 557:9-18. 2013..Altogether, the physiology, pharmacology and therapeutic opportunities surrounding AMPK make it an attractive target for novel intervention for chronic pain and its prevention...
- ZIPping to pain relief: the role (or not) of PKMζ in chronic painTheodore J Price
Department of Pharmacology, The University of Arizona School of Medicine, Arizona, USA
Mol Pain 9:6. 2013....
- Decreased nociceptive sensitization in mice lacking the fragile X mental retardation protein: role of mGluR1/5 and mTORTheodore J Price
McGill University, Anesthesia Research Unit, Faculty of Dentistry and McGill Centre for Research on Pain, Montreal, Quebec, Canada H3G 1Y6
J Neurosci 27:13958-67. 2007..These observations also support the hypothesis that the persistence of self-injurious behavior observed in fragile X mental retardation patients could be related to deficits in nociceptive sensitization...
- Chloride regulation in the pain pathwayTheodore J Price
University of Arizona, Department of Pharmacology, USA
Brain Res Rev 60:149-70. 2009....
- Translating nociceptor sensitivity: the role of axonal protein synthesis in nociceptor physiologyTheodore J Price
The University of Arizona, School of Medicine, Department of Pharmacology, 1501 N Campbell Ave, Tucson, AZ 85724, USA
Eur J Neurosci 29:2253-63. 2009..We believe that an increased understanding of this process will lead to the identification of novel targets for the treatment of chronic pain...
- Fragile X mental retardation protein (FMRP) and the spinal sensory systemTheodore J Price
Department of Pharmacology, The University of Arizona School of Medicine, Tucson, AZ, USA
Results Probl Cell Differ 54:41-59. 2012....
- Spinal protein kinase M ζ underlies the maintenance mechanism of persistent nociceptive sensitizationMarina N Asiedu
Department of Pharmacology, The University of Arizona College of Medicine, Tucson, AZ 85721, USA
J Neurosci 31:6646-53. 2011....
- Development of highly potent protease-activated receptor 2 agonists via synthetic lipid tetheringAndrea N Flynn
Department of Physiology, Arizona Health Sciences Center, Tucson, AZ 85724 5030, USA
FASEB J 27:1498-510. 2013..Our results demonstrate that the STL approach is a powerful tool for increasing ligand potency at PAR₂ and represent opportunities for drug development at other protease activated receptors and across GPCRs...
- BDNF regulates atypical PKC at spinal synapses to initiate and maintain a centralized chronic pain stateOhannes K Melemedjian
Department of Pharmacology, The University of Arizona School of Medicine, Tucson, AZ, USA
Mol Pain 9:12. 2013..Here we have tested the hypothesis that brain derived neurotrophic factor (BDNF) regulates PKMζ, and possibly other aPKCs, to maintain a centralized chronic pain state...
- Targeting adenosine monophosphate-activated protein kinase (AMPK) in preclinical models reveals a potential mechanism for the treatment of neuropathic painOhannes K Melemedjian
Department of Pharmacology, University of Arizona, N Campbell Ave, Tucson, 85724, USA
Mol Pain 7:70. 2011..Therefore, injury-induced dysregulation of translation control underlies pathology leading to neuropathic pain and reveals AMPK as a novel therapeutic target for the potential treatment of neuropathic pain...
- mTORC1 inhibition induces pain via IRS-1-dependent feedback activation of ERKOhannes K Melemedjian
Department of Pharmacology, University of Arizona, Tucson, AZ, USA
Pain 154:1080-91. 2013..Our findings highlight the physiological relevance of feedback signaling through mTORC1 inhibition and have important implications for development of pain therapeutics that target the mTOR pathway...
- Contribution of PKMζ-dependent and independent amplification to components of experimental neuropathic painTamara King
Department of Pharmacology, University of Arizona, Tucson, AZ 85724, USA
Pain 153:1263-73. 2012..In the spinal cord, however, both PKMζ-dependent and independent mechanisms contribute to amplification of evoked responses, but apparently not spontaneous pain...
- The protease-activated receptor-2-specific agonists 2-aminothiazol-4-yl-LIGRL-NH2 and 6-aminonicotinyl-LIGRL-NH2 stimulate multiple signaling pathways to induce physiological responses in vitro and in vivoAndrea N Flynn
Department of Physiology, BIO5 Collaborative Research Institute, Arizona Respiratory Center, Arizona Health Sciences Center, Tucson, Arizona 85724, USA
J Biol Chem 286:19076-88. 2011..We have characterized three high potency ligands that can be used to explore the physiological role of PAR(2) in a variety of systems and pathologies...
- Resveratrol engages AMPK to attenuate ERK and mTOR signaling in sensory neurons and inhibits incision-induced acute and chronic painDipti V Tillu
Department of Pharmacology, University of Arizona, 1501 N Campbell Ave, PO Box 245050, Tucson, AZ 85724, USA
Mol Pain 8:5. 2012....
- Local translation and retrograde axonal transport of CREB regulates IL-6-induced nociceptive plasticityOhannes K Melemedjian
Department of Pharmacology, The University of Arizona School of Medicine, Tucson, USA
Mol Pain 10:45. 2014..Collectively, these findings point to a novel mechanism of axonal translation and retrograde trafficking linking locally-generated signals to long-term nociceptive sensitization. ..
- Development and evaluation of small peptidomimetic ligands to protease-activated receptor-2 (PAR2) through the use of lipid tetheringScott Boitano
Arizona Respiratory Center and Department of Physiology, University of Arizona, Tucson, Arizona, United States of America The BIO5 Collaborative Research Institute, University of Arizona, Tucson, Arizona, United States of America
PLoS ONE 9:e99140. 2014..Using the lipid-tethered-peptidomimetic approach we have developed novel structure activity relationships for PAR2 that allows for selective probing of PAR2 function across a broad range of physiological systems...
- Modulation of spinal GABAergic analgesia by inhibition of chloride extrusion capacity in miceMarina N Asiedu
Department of Pharmacology, The University of Arizona School of Medicine, Tucson, AZ 85724, USA
J Pain 13:546-54. 2012..These results indicate that the KCC2-dependent Cl(-) extrusion capacity differentially regulates the analgesic efficacy of agonists and allosteric modulators at the GABA(A) receptor complex...
- Sensitization of dural afferents underlies migraine-related behavior following meningeal application of interleukin-6 (IL-6)Jin Yan
Department of Pharmacology, University of Arizona College of Medicine, 1501 N Campbell Ave, PO Box 245050, Tucson, AZ 85724, USA
Mol Pain 8:6. 2012..Intracranial interleukin-6 (IL-6) levels have been shown to be elevated during migraine attacks, suggesting that this cytokine may facilitate pain signaling from the meninges and contribute to the development of headache...
- Lanthanide labeling of a potent protease activated receptor-2 agonist for time-resolved fluorescence analysisJustin Hoffman
Department of Physiology, Arizona Health Sciences Center, 1501 North Campbell Avenue, Tucson, AZ 85724 5030, USA
Bioconjug Chem 23:2098-104. 2012..This ligand can serve as a critical tool in the screening and development of PAR(2) ligands...
- Engagement of descending inhibition from the rostral ventromedial medulla protects against chronic neuropathic painMilena De Felice
Department of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ 85724, USA
Pain 152:2701-9. 2011..Engagement of descending inhibition protects in the transition from acute to chronic pain. These unexpected findings might provide a mechanistic explanation for medications that engage descending inhibition or mimic its consequences...
- Neuroligin 2 regulates spinal GABAergic plasticity in hyperalgesic priming, a model of the transition from acute to chronic painJi Young V Kim
aDepartment of Pharmacology, University of Arizona, Tucson, AZ, USA bSchool of Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, TX, USA cBio5 Institute, University of Arizona, Tucson, AZ, USA
Pain 157:1314-24. 2016..Our observations reveal new mechanisms involved in the spinal maintenance of a pain plasticity and further suggest that disinhibitory mechanisms are central features of neuroplasticity in the spinal dorsal horn. ..
- IL-6- and NGF-induced rapid control of protein synthesis and nociceptive plasticity via convergent signaling to the eIF4F complexOhannes K Melemedjian
Department of Pharmacology, University of Arizona School of Medicine, Tucson, Arizona 85724, USA
J Neurosci 30:15113-23. 2010..These results establish IL-6- and NGF-mediated cap-dependent translation of local proteins as a new model for nociceptive plasticity...
- Spinal dopaminergic projections control the transition to pathological pain plasticity via a D1/D5-mediated mechanismJi Young V Kim
Department of Pharmacology, University of Arizona, Tucson, Arizona 85721
J Neurosci 35:6307-17. 2015..These findings demonstrate a novel role for descending dopaminergic neurons in the maintenance of pathological pain plasticity. ..
- Contrasting effects of chronic, systemic treatment with mTOR inhibitors rapamycin and metformin on adult neural progenitors in miceYael Kusne
Neuroscience Graduate Program, Arizona State University, Phoenix, AZ, 85287, USA
Age (Dordr) 36:199-212. 2014..These results underscore the importance of screening individual mTOR inhibitors on different organs and physiological processes for potential adverse effects that may compromise health span. ..
- Competing molecular interactions of aPKC isoforms regulate neuronal polaritySara S Parker
Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ 85724, USA
Proc Natl Acad Sci U S A 110:14450-5. 2013..In contrast, the overexpression of PKM-ζ prevents axon specification. Our studies suggest a molecular model wherein mutually antagonistic intermolecular competition between aPKC isoforms directs the establishment of neuronal polarity. ..
- Role of cation-chloride-cotransporters (CCC) in pain and hyperalgesiaTheodore J Price
Anesthesia Research Unit Faculty of Medicine, Faculty of Dentistry and McGill Center for Pain Research McGill University, Montreal, Quebec, Canada
Curr Top Med Chem 5:547-55. 2005..Pharmacological targeting of these cation chloride cotransporters to restore normal GABA-/glycinergic transmission in the spinal cord represents an entirely novel approach to the development of analgesics...
- Critical evaluation of the colocalization between calcitonin gene-related peptide, substance P, transient receptor potential vanilloid subfamily type 1 immunoreactivities, and isolectin B4 binding in primary afferent neurons of the rat and mouseTheodore J Price
Department of Pharmacology, The University of Texas Health Science Center at San Antonio San Antonio, TX, USA
J Pain 8:263-72. 2007..Thus, whereas only an approximately 10% overlap was observed in TG neurons of mouse, significantly greater overlap (approximately 35%) was observed in those of rat...
- Spinal NKCC1 blockade inhibits TRPV1-dependent referred allodyniaMark H Pitcher
McGill University, Anesthesia Research Unit, Faculty of Medicine, Faculty of Dentistry and McGill Centre for Research on Pain, Montreal, QC, Canada
Mol Pain 3:17. 2007..TRPV1 receptors transduce diverse chemical and natural stimuli in nociceptors and are critical for inflammatory hyperalgesia...
- Reversal of pancreatitis-induced pain by an orally available, small molecule interleukin-6 receptor antagonistMarina Vardanyan
Department of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ 85724, USA
Pain 151:257-65. 2010..Strategies targeting IL-6 actions through small molecule antagonists may offer novel approaches to improve the therapy of chronic pancreatitis and other chronic pain states...
- Ensuring transparency and minimization of methodologic bias in preclinical pain research: PPRECISE considerationsNick A Andrews
aDepartment of Neurobiology, Boston Children s Hospital, Harvard Medical School, Boston, MA, USA bDepartment of Anatomy, University of California San Francisco, San Francisco, CA, USA cDepartment of Psychology and Alan Edwards Centre for Research on Pain, McGill University, Montreal, Canada dDepartment of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ, USA ePain Research, Department of Surgery and Cancer, Imperial College, London, United Kingdom fCentre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom Departments of gAnesthesiology, hNeurology, and iPsychiatry, University of Rochester, Rochester, NY, USA jDepartment of Anesthesiology, Wake Forest School of Medicine, Winston Salem, NC, USA kDepartment of Biostatistics, Harvard University, Boston, MA, USA lDepartment of Anesthesiology, University of Rochester, Rochester, NY, USA mClinical and Rehabilitative Medicine Research Program, United States Army Medical Research and Materiel Command, Fort Detrick, MD, NJ 08903-0231
Pain 157:901-9. 2016..We believe that to achieve the goal of finding effective new treatments for patients with pain, the pain field needs to deal with these challenging issues...
- A highly potent agonist to protease-activated receptor-2 reveals apical activation of the airway epithelium resulting in Ca2+-regulated ion conductanceCara L Sherwood
Arizona Respiratory Center, University of Arizona, Tucson, Arizona The BIO5 Collaborative Research Institute, University of Arizona, Tucson, Arizona
Am J Physiol Cell Physiol 307:C718-26. 2014..Stimulation of Cl(-) efflux via PAR2 activation at the airway epithelial surface can increase airway surface liquid that would aid in clearing the airway of noxious inhaled agents. ..
- Inhibition of carbonic anhydrase augments GABAA receptor-mediated analgesia via a spinal mechanism of actionMarina N Asiedu
Department of Pharmacology, The University of Arizona School of Medicine, Tucson, Arizona
J Pain 15:395-406. 2014..We suggest that carbonic anhydrase inhibitors, many of which are clinically available, might be advantageously employed for the treatment of pathologic pain states...
- Protein expression and mRNA cellular distribution of the NKCC1 cotransporter in the dorsal root and trigeminal ganglia of the ratTheodore J Price
McGill University, Departments of Anesthesia and Dentistry and McGill Centre for Research on Pain, 3655 Prom Sir William Osler, Montreal, QC, Canada H3G 1Y6
Brain Res 1112:146-58. 2006..Moreover, these results suggest the possibility of a functional role of NKCC1 in the glial cells closely apposed to primary sensory afferents...
- Proteomic and functional annotation analysis of injured peripheral nerves reveals ApoE as a protein upregulated by injury that is modulated by metformin treatmentOhannes K Melemedjian
Department of Pharmacology, The University of Arizona School of Medicine, 1501 N Campbell Ave, Tucson, AZ 85724, USA
Mol Pain 9:14. 2013....
- The AMPK Activator A769662 Blocks Voltage-Gated Sodium Channels: Discovery of a Novel Pharmacophore with Potential Utility for Analgesic DevelopmentMarina N Asiedu
University of Arizona, Department of Pharmacology, Tucson, Arizona, United States of America
PLoS ONE 12:e0169882. 2017..These data indicate that in addition to AMPK activation, A769662 acts as a direct blocker/modulator of VGSCs, a potential mechanism enhancing the analgesic property of this compound...
- Pharmacogenetic inhibition of eIF4E-dependent Mmp9 mRNA translation reverses fragile X syndrome-like phenotypesChristos G Gkogkas
Department of Biochemistry and Goodman Cancer Research Centre, McGill University, Montreal, QC H3A 1A3, Canada Electronic address
Cell Rep 9:1742-55. 2014..These results uncover a mechanism of regulation of synaptic function by translational control of Mmp-9 in FXS, which opens the possibility of new treatment avenues for the diverse neurological and psychiatric aspects of FXS. ..
- Acetazolamide and midazolam act synergistically to inhibit neuropathic painMarina Asiedu
The University of Arizona School of Medicine, Department of Pharmacology, Tucson, AZ 85724, USA
Pain 148:302-8. 2010..These findings indicate that the combined use of CA inhibitors and benzodiazepines may be effective in the clinical management of neuropathic pain in humans...
- Oestrogen receptors interact with the α-catalytic subunit of AMP-activated protein kinaseYulia Lipovka
Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85724, U S A Department of Physiology, University of Arizona, Tucson, AZ 85724, U S A
Biosci Rep 35:. 2015..We conclude that E2 activates AMPK through ERα by direct interaction with the βγ-binding domain of AMPKα...
- Bidirectional regulation of P body formation mediated by eIF4F complex formation in sensory neuronsOhannes K Melemedjian
Department of Pharmacology, University of Arizona, Tucson, AZ, United States Electronic address
Neurosci Lett 563:169-74. 2014..These studies indicate that P body formation is intricately linked to cap-dependent translation in mammalian sensory neurons suggesting an important role for these organelles in the regulation of mRNA metabolism in the adult PNS. ..
- Potent agonists of the protease activated receptor 2 (PAR2)Scott Boitano
Arizona Respiratory Center and Department of Physiology, University of Arizona, 1501 N Campbell Avenue, Tucson, Arizona 85724, United States
J Med Chem 54:1308-13. 2011..Together these will lead to discovery of more potent agonists and antagonists of PAR(2)...
- The cannabinoid WIN 55,212-2 inhibits transient receptor potential vanilloid 1 (TRPV1) and evokes peripheral antihyperalgesia via calcineurinAmol M Patwardhan
Department of Pharmacology, University of Texas Health Science Center, San Antonio, TX 78229, USA
Proc Natl Acad Sci U S A 103:11393-8. 2006..Collectively, these data demonstrate that cannabinoids such as WIN directly inhibit TRPV1 functional activities via a calcineurin pathway that represents a mechanism of cannabinoid actions at peripheral sites...
- Pharmacological interactions between calcium/calmodulin-dependent kinase II alpha and TRPV1 receptors in rat trigeminal sensory neuronsTheodore J Price
The University of Texas Health Science Center at San Antonio, Department of Endodontics, 7703 Floyd Curl Dr, San Antonio, TX 78229, USA
Neurosci Lett 389:94-8. 2005....
- Chloride cation co-transporters and hyperalgesic statesTHEODORE PRICE; Fiscal Year: 2007..These hypotheses comprise an integrated series of studies that test hypotheses concerning Abeta-fiber driven pain leading to possible therapeutic strategies for the alleviation of inflammatory pain. ..