Susan M. Carlton, Ph.D. Professor
- Affiliations: Department of Neuroscience & Cell Biology
- Route: 1069, 2.138 Medical Research Building (MRB)
- Tel: (409) 772-1703
- Fax: (409) 762-9382
Susan M. Carlton, Ph.D.
B.S. in Biology, University of Mary Washington, Fredericksburg, VA, 1977
Ph.D. in Anatomy, Medical College of Virginia, Richmond, VA, 1982
Postdoctoral Fellow, Marine Biomedical Institute, UTMB, 1982-1985
Postdoctoral Fellow, Yale University, School of Medicine, 1985
My research activities focus on the analysis of neuroplasticity that underlies chronic pain. In one line of research, we are elucidating those receptors involved in the processing of nociceptive (painful) input in the periphery. Then, using models of inflammation coupled with anatomical, behavioral, pharmacological and electrophysiological techniques, we investigate how these receptor populations change in acute and chronic inflammation. We are particularly interested in the role of ionotropic and metabotropic glutamate receptors as will as somatostatin and TRPV1 receptors which are expressed by cutaneous nociceptors. It is becoming clear that a variety of receptors are present on peripheral axons that influence sensory transduction in the normal state and contribute to enhanced nociceptor function in the inflamed state. Investigating neuronal receptor populations in normal skin and changes in these populations in chronic pain states may elucidate new avenues for therapy for pain of peripheral origin.
A second focus in the lab is the study of mechanisms underlying both peripheral and central neuropathic pain. Using models of peripheral nerve injury or spinal cord contusion, we are defining those mechanisms contributing to the aberrant sensory processing that arises following PNS or CNS injury, respectively. We have demonstrated that a CNS injury (spinal cord contusion) results in sensitization of primary afferents far from the injury site. This finding may have implications for other painful conditions such as fibromyalgia, thalamic post-stroke pain and migraine pain.
Publications (selected from 108)
Carlton, S.M., Zhou, S., Du, J., Hargett, G. L., Ji, Guangchen, and Coggeshall, R.E, Somatostatin modulates the transient receptor potential vanilloid 1 (TRPV1) ion channel, Pain, 110:616-627, 2004.
Palecek, J., Neugebauer, V., Carlton, S.M., Iyengar, S., and Willis, W.D., The effect of kainate GluR5 receptor antagonist on responses of spinothalamic tract neurons in a model of peripheral neuropathy in primates, Pain, 111:151-161, 2004.
Jimenez-Andrade, J. M., Zhou, S., Yamani, A., Valencia de Ita, S., Castaneda-Hernandez, G. and Carlton, S. M. Mechanisms by which peripheral galanin increases acute inflammatory pain, Brain Research, 1056, 113-117, 2005.
Du, J., Zhou, S., and Carlton, S.M. Kainate-induced excitation of nociceptors in normal and inflamed rat glabrous skin, Neuroscience, 137: 999-1013, 2006.
Ji, G., Zhou, S., Shapiro, G., Reubi, J.C., Jurczyk, S., Carlton, S.M., Analgesic activity of a non-peptide imidazolidinedione somatostatin agonist: in vitro and in vivo studies in rat, Pain 124: 34-49, 2006.
Jimenez-Andrade, J.M., Lundstrom, L., Sollenberg, U.E., Langel, U., Castaneda-Hernandez, G., Carlton, S.M., Activation of peripheral galanin receptors: Differential effects on nociception. Pharm. Biochem. Behav. 85: 273-280, 2006.
Carlton, S.M., and Hargett, G.L. Co-localization of metabotropic glutamate receptors in rat dorsal root ganglion cells. J. Comp. Neurol. 501: 780-789, 2007.
Ji, G, Zhou, S. Kochukov, M., High, K.N. and Carlton, S.M., Plasticity in intact A-delta fibers contributes to cold hypersensitivity in neuropathic pain. Neuroscience 150: 182-193, 2007.
Ji, G, Zhou, S and Carlton, S.M., Intact Ad-fibers up-regulate TRPA1 and contribute to cold hypersensitivity in neuropathic rats. Neuroscience, 154: 754-766, 2008.
Du, J, Zhou, S. and Carlton, S.M., Group II metabotropic glutamate receptor activation attenuates peripheral sensitization in inflammatory states. Neuroscience, 154:1054-1066, 2008.