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Molecular underpinnings of ventral surface chemoreceptor function: focus on KCNQ channels
Author(s) -
Mulkey Daniel K.,
Hawkins Virginia E.,
Hawryluk Joanna M.,
Takakura Ana C.,
Moreira Thiago S.,
Tzingounis Anastasios V.
Publication year - 2015
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2014.286500
Subject(s) - chemoreceptor , neuroscience , serotonergic , epilepsy , biology , control of respiration , respiratory system , serotonin , receptor , anatomy , biochemistry
Central chemoreception is the mechanism by which CO 2 /H + ‐sensitive neurons (i.e. chemoreceptors) regulate breathing in response to changes in tissue CO 2 /H + . Neurons in the retrotrapezoid nucleus (RTN) directly regulate breathing in response to changes in tissue CO 2 /H + and function as a key locus of respiratory control by integrating information from several respiratory centres, including the medullary raphe. Therefore, chemosensitive RTN neurons appear to be critically important for maintaining breathing, thus understanding molecular mechanisms that regulate RTN chemoreceptor function may identify therapeutic targets for the treatment of respiratory control disorders. We have recently shown that KCNQ (Kv7) channels in the RTN are essential determinants of spontaneous activity ex vivo , and downstream effectors for serotonergic modulation of breathing. Considering that loss of function mutations in KCNQ channels can cause certain types of epilepsy including those associated with sudden unexplained death in epilepsy (SUDEP), we propose that dysfunctions of KCNQ channels may be one cause for epilepsy and respiratory problems associated with SUDEP. In this review, we will summarize the role of KCNQ channels in the regulation of RTN chemoreceptor function, and suggest that these channels represent useful therapeutic targets for the treatment of respiratory control disorders.