2024-03-29T07:40:14Zhttp://uvadoc.uva.es/oai/requestoai:uvadoc.uva.es:10324/68902022-07-29T08:21:24Zcom_10324_1134com_10324_931com_10324_894col_10324_1213
Liu, X.
He, Le
Dinger, Bruce
González, Constancio
Stensaas, L.
Fidone, Salvatore
2011
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
http://uvadoc.uva.es/handle/10324/6890
eng
Elsevier
Neurofisiología
Dolor crónico - Tratamiento
A chronic pain: inflammation-dependent chemoreceptor adaptation in rat carotid body
info:eu-repo/semantics/article
TEXT
UVaDOC. Repositorio Documental de la Universidad de Valladolid
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