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Liu, X. He, Le Dinger, Bruce González Martínez, Constancio Stensaas, L. Fidone, Salvatore 2014-11-04T09:39:49Z 2014-11-04T09:39:49Z 2011 Respiratry Physiology and Neurobiology : 2011, 178(3) 362-369 1569-9048 http://uvadoc.uva.es/handle/10324/6890 10.1016/j.resp.2011.03.006 362 178 369 Respiratory Physiology and Neurobiology Producción Científica Experiments in recent years have revealed labile electrophysiological and neurochemical phenotypes in primary afferent neurons exposed to specific stimulus conditions associated with the development of chronic pain. These studies collectively demonstrate that the mechanisms responsible for functional plasticity are primarily mediated by novel neuroimmune interactions involving circulating and resident immune cells and their secretory products, which together induce hyperexcitability in the primary sensory neurons. In another peripheral sensory modality, namely the arterial chemoreceptors, sustained stimulation in the form of chronic hypoxia (CH) elicits increased chemoafferent excitability from the mammalian carotid body. Previous studies which focused on functional changes in oxygen-sensitive type I cells in this organ have only partially elucidated the molecular and cellular mechanisms which initiate and control this adaptive response. Recent studies in our laboratory indicate a unique role for the immune system in regulating the chemo-adaptive response of the carotid body to physiologically relevant levels of hypoxia. application/pdf eng Elsevier info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-nd/4.0/ Attribution-NonCommercial-NoDerivatives 4.0 International Neurofisiología Dolor crónico - Tratamiento A chronic pain: inflammation-dependent chemoreceptor adaptation in rat carotid body info:eu-repo/semantics/article https://www.sciencedirect.com/science/article/pii/S1569904811000887 SI