References:
- Walters ET, Bodnarova M, Dulin MF, Diaz-Rios M, Miller MW, Moroz LL (2004) Somatotopic organization and functional properties of mechanosensory neurons expressing sensorin-A mRNA in Aplysia californica. J Comp Neurol 471:219-240.
- Sung, Y. J., E. T. Walters and R. T. Ambron (2004). Retrograde axonal transport of a neuronal isoform of PKG couples MAPK nuclear import to axotomy-induced long-term hyperexcitability in Aplysia sensory neurons. J Neurosci, 24:7583-7595.
- Weragoda RMS, Ferrer E, Walters ET (2004) Memory-like alterations in Aplysia axons following localized nerve depolarization or injury. 24:10393-10401.
- Gasull, X., Liao, X., Dulin, M.F., Phelps, C., Walters, E.T. (2005) Evidence that long-term hyperexcitability of the sensory neuron soma induced by nerve injury is adaptive. J. Neurophysiol. 3:2218-2230.
- Song, XJ, Wang, ZB, Gan, Q, Walters, ET (2006) cAMP and cGMP contribute to sensory neuron hyperexcitability and hyperalgesia in rats with dorsal root ganglia compression. J Neurophysiol, 95:479-492.
- Zheng, JH, Walters, ET, Song, XJ (2006) Dissociation of dorsal root ganglion neurons induces hyperexcitability that is maintained by increased responsiveness to cAMP and cGMP. J Neurophysiol, 97:15-25.
- Weragoda, R.M.S., Walters, E.T. (2007) Serotonin induces memory-like, rapamycin-sensitive hyperexcitability in sensory axons of Aplysia that contributes to injury responses. J. Neurophysiol, 98:1231-1239.
Edgar T. Walters, Ph.D.
Professor
UTHSC-Medical School, (713) 500 - 6314
Edgar.T.Walters@uth.tmc.edu
Neuronal injury, pain, and memory
We explore adaptive responses of neurons to injury and stress, and potentially ancient links between these responses and mechanisms important for pain and memory. Some of our work utilizes a large marine snail, Aplysia, whose large, accessible neurons enable single-cell experimental manipulations (electrical and molecular) and which allow us to define the role of individual cells and their alterations in an animal’s behavior. For example, intracellular injection has been used to investigate contributions of the cAMP-PKA-CREB and NO-cGMP-PKG pathways to long-term hyperexcitability of the cell bodies of nociceptors. Electrophysiological and pharmacological methods are being used to study contributions of local, rapamycin-sensitive protein synthesis to long-term hyperexcitability of the axons of nociceptors. A novel discovery is that long-term axonal hyperexcitability can be induced by mechanisms that depend upon local depolarization but not calcium signals. New studies are examining long-term hyperexcitability in nociceptors of the rat following spinal cord injury and other stresses. Researchers in our lab are utilizing three preparations that provide complementary advantages for exploring fundamental mechanisms and functions of injury-related plasticity: rat dorsal root ganglion neurons, Aplysia nociceptors and motor neurons, and the giant axon of the squid. We combine various techniques, including controlled intracellular or extracellular delivery of cellular messengers or their antagonists, whole-cell and axial voltage clamping, light and electron microscopy, cell and organ culture methods, in situ hybridization, biochemical assays, and sophisticated methods for probing behavioral responses of invertebrate and vertebrate animals.
