Neuron-Glia Crosstalk in the Autonomic Nervous System and Its Possible Role in the Progression of Metabolic Syndrome: A New Hypothesis
Date
2015
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Article
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Abstract
Metabolic 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.
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Citation
Del Rio R, Quintanilla RA, Orellana JA, Retamal MA. Neuron-Glia Crosstalk in the Autonomic Nervous System and Its Possible Role in the Progression of Metabolic Syndrome: A New Hypothesis. Front Physiol. 2015 Dec 1;6:350
Keywords
Glia, Connexins, Metabolic syndrome, Mitochondria, Tripartite synapse, Hemichannels