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Neuron-Glia crosstalk in the autonomic nervous system and its possible role in the progression of metabolic syndrome: A new hypothesis

dc.contributor.authorRio R.D.
dc.contributor.authorQuintanilla R.A.
dc.contributor.authorOrellana J.A.
dc.contributor.authorRetamal M.A.
dc.date.accessioned2020-09-02T22:27:00Z
dc.date.available2020-09-02T22:27:00Z
dc.date.issued2015
dc.identifier10.3389/fphys.2015.00350
dc.identifier.citation6, DEC, -
dc.identifier.issn1664042X
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6019
dc.descriptionMetabolic syndrome (MS) is characterized by the following physiological alterations: increase in abdominal fat, insulin resistance, high concentration of triglycerides, low levels of HDL, high blood pressure, and a generalized inflammatory state. One of the pathophysiological hallmarks of this syndrome is the presence of neurohumoral activation, which involve autonomic imbalance associated to hyperactivation of the sympathetic nervous system. Indeed, enhanced sympathetic drive has been linked to the development of endothelial dysfunction, hypertension, stroke, myocardial infarct, and obstructive sleep apnea. Glial cells, the most abundant cells in the central nervous system, control synaptic transmission, and regulate neuronal function by releasing bioactive molecules called gliotransmitters. Recently, a new family of plasma membrane channels called hemichannels has been described to allow the release of gliotransmitters and modulate neuronal firing rate. Moreover, a growing amount of evidence indicates that uncontrolled hemichannel opening could impair glial cell functions, affecting synaptic transmission and neuronal survival. Given that glial cell functions are disturbed in various metabolic diseases, we hypothesize that progression of MS may relies on hemichannel-dependent impairment of glial-to-neuron communication by a mechanism related to dysfunction of inflammatory response and mitochondrial metabolism of glial cells. In this manuscript, we discuss how glial cells may contribute to the enhanced sympathetic drive observed in MS, and shed light about the possible role of hemichannels in this process. © 2015 Del Rio, Quintanilla, Orellana and Retamal.
dc.language.isoen
dc.publisherFrontiers Research Foundation
dc.subjectConnexins
dc.subjectGlia
dc.subjectHemichannels
dc.subjectMetabolic syndrome
dc.subjectMitochondria
dc.subjectTripartite synapse
dc.subjectadenosine triphosphatase (potassium sodium)
dc.subjectexcitatory amino acid transporter
dc.subjectglial fibrillary acidic protein
dc.subjectinterleukin 1beta
dc.subjectinwardly rectifying potassium channel
dc.subjectnestin
dc.subjecttumor necrosis factor alpha
dc.subjectvimentin
dc.subjectArticle
dc.subjectastrocyte
dc.subjectautonomic nervous system
dc.subjectcell activation
dc.subjectcell communication
dc.subjectcell function
dc.subjectcell interaction
dc.subjectencephalitis
dc.subjectglia cell
dc.subjectgliosis
dc.subjecthemichannel
dc.subjecthuman
dc.subjecthypothesis
dc.subjectmembrane channel
dc.subjectmetabolic syndrome X
dc.subjectmicroglia
dc.subjectnerve cell
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectparacrine signaling
dc.subjectsympathetic nerve cell
dc.subjectsympathetic tone
dc.subjectsynaptic transmission
dc.titleNeuron-Glia crosstalk in the autonomic nervous system and its possible role in the progression of metabolic syndrome: A new hypothesis
dc.typeArticle


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