Author/Authors :
Bahari، Zahra نويسنده Faculty of Psychology and Social Sciences, Islamic Azad University, Tehran Central Branch , , Sadr، Seyed Shahabeddin نويسنده Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, IR Iran , , Meftahi، Gholam Hossein نويسنده Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, IR Iran , , Ghasemi، Maedeh نويسنده Department of Physiology, Isfahan University of Medical Sciences, Isfahan, IR Iran , , Manaheji، Homa نويسنده , , Mohammadi، Alireza نويسنده , , Mehranfard، Nasrin نويسنده Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, IR Iran ,
Abstract :
Neuropathic pain is a common and disabling complication. To develop a better treatment of the neuropathic pain, a comprehensive understanding is essential. In this paper, we review pathophysiological principles of neuropathic pain, focusing on synaptic plasticity and long-term potentiation (LTP) in the nociceptive circuits. Finally, the role of glial cells on the synaptic plasticity in neuropathic pain is discussed. We searched the Cochrane and PubMed databases using the following terms: neuropathic pain, dorsal horn, LTP, synaptic plasticity, nociceptive circuits, glial cells, nerve injury, allodynia, hyperalgesia, nociceptive neurons, and rat. All of searches were limited to the animal studies in English articles. Full-text copies were obtained when the studies had possible relevance. Analysis of our research showed that nerve injury-induced LTP decreased pain threshold and increased pain hypersensitivity to sub-threshold stimuli. In addition, cross talk between dorsal horn neurons and glial cells are pivotal for the induction of spinal synaptic plasticity and LTP. It seems that LTP in the spinal nociceptive pathways constitutes cellular mechanisms that explains how acute pain may become chronic.
