title: Exercise-induced hypoalgesia: potential mechanisms in animal models of neuropathic pain.
abstract: Physical exercise, such as forced treadmill running and swimming, can sufficiently improve mechanical allodynia and heat hyperalgesia in animal models of neuropathic pain (NPP), including partial sciatic nerve ligation, chronic constriction injury, and spinal nerve ligation models. Thus, physical exercise has been established as a low-cost, safe, and effective way to manage NPP conditions, but the exact mechanisms underlying such exercise-induced hypoalgesia (EIH) are not fully understood. A growing body of evidence has identified several factors that work at different levels of the nervous system as playing important roles in producing EIH in animal models of NPP. The objective of this review is to provide an overview of key players associated with EIH, and then to discuss our current understanding of the mechanisms underlying EIH. Relevant studies have demonstrated that physical exercise can dramatically alter the levels of inflammatory cytokines, neurotrophins, neurotransmitters, endogenous opioids, and histone acetylation at various sites in the nervous system, such as injured peripheral nerves, dorsal root ganglia, and spinal dorsal horn in animal models of NPP, thereby contributing to the production of EIH. These results suggest that EIH is produced through multiple cellular and molecular events in the pain pathway.
authors.affiliation: Department of Rehabilitation Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama City, Wakayama, 641-8509, Japan. kami@wakayama-med.ac.jp.
authors.forename: Katsuya
authors.initials: K
authors.lastname: Kami
authors.affiliation: Department of Rehabilitation Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama City, Wakayama, 641-8509, Japan.
authors.forename: Fumihiro
authors.initials: F
authors.lastname: Tajima
authors.affiliation: Department of Rehabilitation Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama City, Wakayama, 641-8509, Japan.|Department of Physical Therapy, Osaka Yukioka College of Health Science, 1-1-41 Sojiji, Ibaraki City, Osaka, 567-0801, Japan.
authors.forename: Emiko
authors.initials: E
authors.lastname: Senba
mesh_terms: D000107:Acetylation; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D015444:Exercise / Q000502:physiology*; D059330:GABAergic Neurons; D006657:Histones; D006801:Humans; D006930:Hyperalgesia / Q000628:therapy; D018836:Inflammation Mediators / Q000378:metabolism; D009414:Nerve Growth Factors / Q000378:metabolism; D009420:Nervous System / Q000378:metabolism; D009437:Neuralgia / Q000628:therapy*; D018377:Neurotransmitter Agents / Q000378:metabolism; D018847:Opioid Peptides / Q000378:metabolism
chemical_list: D016207:Cytokines; D006657:Histones; D018836:Inflammation Mediators; D009414:Nerve Growth Factors; D018377:Neurotransmitter Agents; D018847:Opioid Peptides
keywords: Epigenetics; Exercise-induced hypoalgesia; GABAergic neuron; Histone acetylation; Neuropathic pain