WJNS  Vol.3 No.1 , February 2013
Pain and memory: Do they share similar mechanisms?
Author(s) Merab G. Tsagareli*
ABSTRACT

Pain receptors, nociceptors inputs to the spinal cord and supra spinal structures triggering a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, is the phenomenon of central sensitization. Key processes for pain memory stabilizing could be considering processes of peripheral and central sensitizations. Mechanical hypersensitivity and allodynia to light touch after central sensitization are pathologic in that they are evoked by Aβ low threshold mechanoreceptors, which normally do not produce painful sensations. Peripheral sensitization allows low-intensity stimuli to produce pain by activating Aδ and C nociceptors whereas central sensitization allows normal low-threshold Aβ mechanoreceptors to produce pain as a result of changes in sensory processing in the spinal cord. During peripheral and central sensitization, the receptive fields of dorsal horn neurons expand beyond the site of injury into surrounding non-injured tissue. The clinical result of all above changes is hyperalgesia, allodynia, spontaneous pain, referred pain and sym-pathetically maintained pain. Therefore, these persistent sensory responses to noxious stimuli are a form of memory, the memory for pain. Long lasting synaptic plasticity as the long-term potentialtion at spinal and supra-spinal levels could undergo hyperalgesia and allodynia. The latter could be providing neuronal basis for persistent pain and pain memory. Thus, it will be particularly important to know how to regulate long-lasting plastic changes in spinal cord, thalamus and cortex. Molecular mechanisms of these plastic processes could be main targets for new therapeutic drugs in pain relief.


Cite this paper
Tsagareli, M. (2013) Pain and memory: Do they share similar mechanisms?. World Journal of Neuroscience, 3, 39-48. doi: 10.4236/wjns.2013.31005.
References
[1]   Woolf, C.J. (2011) Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152, S2-S15. doi:10.1016/j.pain.2010.09.030

[2]   Walters, E.T. (2009) Evolutionary aspects of pain. In: Basbaum, A.I. and Bushnell, M.C., Eds., Science of Pain, Elsevier, San Diego, 175-184.

[3]   Brunelli, M., Castellucci, V. and Kandel, E.R. (1976) Synaptic facilitation and behavioral sensitization in Aplysia: Possible role of serotonin and cyclic AMP. Science, 194, 1178-1181. doi:10.1126/science.186870

[4]   Squire, L.R. and Kandel, E.R. (2009) Memory: From mind to molecules. 2nd Edtion, Roberts & Company, Greenwood Village.

[5]   Thompson, S.W., Woolf, C.J., Sivilotti, L.G. (1993) Small-caliber afferent inputs produce a heterosynaptic facilitation of the synaptic responses evoked by primary afferent A-fibers in the neonatal rat spinal cord in vitro. Journal of Neurophysiology, 69, 2116-28.

[6]   Bliss, T.V.P. and Collingridge, G.L. (1993) A synaptic model of memory: Long-term potentiation in the hippo-campus. Nature, 361, 31-39. doi:10.1038/361031a0

[7]   Malenka, R.C. and Nicoll, R.A. (1999) Long-term potentiation—A decade of progress? Science, 285, 1870-1874. doi:10.1126/science.285.5435.1870

[8]   Neves, G., Cook, S.F. and Bliss, T.V. (2008) Synaptic plasticity, memory and the hippocampus: A neural network approach to causality. Nature Reviews of Neuroscience, 9, 65-75. doi:10.1038/nrn2303

[9]   LeDoux, J.E. (2000) Emotional circuits in the brain. Annual Reviews of Neuroscience, 23, 155-184. doi:10.1146/annurev.neuro.23.1.155

[10]   Maren, S. (2005) Synaptic mechanisms of associative memory in the amygdala. Neuron, 47, 783-786. doi:10.1016/j.neuron.2005.08.009

[11]   Phelps, E.A. and Le Doux, J.E. (2005) Contribution of the amygdala to emotion processing: From animal models to human behavior. Neuron, 48, 175-187. doi:10.1016/j.neuron.2005.09.025

[12]   Sigurdsson, T., Doyère, V., Cain, C.K. and LeDoux, J.E. (2007) Long-term potentiation in the amygdala: A cellular mechanism of fear learning and memory. Neuropharmacology, 51, 215-227. doi:10.1016/j.neuropharm.2006.06.022

[13]   Sandkühler, J. (2009) Long-term potentiation in pain pathways. In: Basbaum, A.I. and Bushnell, M.C., Eds., Science of Pain, Elsevier, San Diego, 401-406.

[14]   Woolf, C.J. and Salter, M.W. (2006) Plasticity and pain: Role of the dorsal horn. In: McMahon, S.B. and Koltzenburg, M., Eds., Wall & Melzack’s Textbook of Pain, Elsevier, London, 91-105.

[15]   Willis, W.D. (2002) Long-term potentiation in spinothalamic neurons. Brain Research Reviews, 40, 202-214. doi:10.1016/S0165-0173(02)00202-3

[16]   Zhuo, M. (2007) Neuronal mechanism for neuropathic pain. Molecular Pain, 3, 14-23. doi:10.1186/1744-8069-3-14

[17]   Shyu, B.-C. and Vogt, B.A. (2009) Short-term synaptic plasticity in the nociceptive thalamic anterior cingulate cortex. Molecular Pain, 5, 51-71. doi:10.1186/1744-8069-5-51

[18]   Wei, F. and Zhuo, M. (2001) Potentiation of sensory responses in the anterior cingulate cortex following digit amputation in the anaesthetized rat. The Journal of Physiology, 532, 823-833. doi:10.1111/j.1469-7793.2001.0823e.x

[19]   Zhuo, M. (2007) A synaptic model for pain: Long-term potentiation in the anterior cingulate cortex. Molecules and Cells, 23, 259-271.

[20]   Drdla-Schutting, R., Benrath, J., Wunderbaldinger, G. and Sandkühler, J. (2012) Erasure of a spinal memory trace of pain by a brief, high-dose opioid administration. Science, 335, 235-238. doi:10.1126/science.1211726

[21]   Latremoliere, A. and Woolf, C.J. (2009) Central sensitization: A generator of pain hypersensitivity by central neural plasticity. The Journal of Pain, 10, 895-926. doi:10.1016/j.jpain.2009.06.012

 
 
Top