Molecular underpinnings of ventral surface chemoreceptor function: focus on KCNQ channels
Central chemoreception is the mechanism by which CO2/H+‐sensitive neurons (i.e. chemoreceptors) regulate breathing in response to changes in tissue CO2/H+. Neurons in the retrotrapezoid nucleus (RTN) directly regulate breathing in response to changes in tissue CO2/H+ and function as a key locus of r...
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| Published in: | The Journal of physiology Vol. 593; no. 5; pp. 1075 - 1081 |
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| Abstract | Central chemoreception is the mechanism by which CO2/H+‐sensitive neurons (i.e. chemoreceptors) regulate breathing in response to changes in tissue CO2/H+. Neurons in the retrotrapezoid nucleus (RTN) directly regulate breathing in response to changes in tissue CO2/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. |
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| AbstractList | Central chemoreception is the mechanism by which CO2/H+-sensitive neurons (i.e. chemoreceptors) regulate breathing in response to changes in tissue CO2/H+. Neurons in the retrotrapezoid nucleus (RTN) directly regulate breathing in response to changes in tissue CO2/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. 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. Central chemoreception is the mechanism by which CO₂/H(+) -sensitive neurons (i.e. chemoreceptors) regulate breathing in response to changes in tissue CO₂/H(+) . Neurons in the retrotrapezoid nucleus (RTN) directly regulate breathing in response to changes in tissue CO₂/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. |
| Author | Hawkins, Virginia E. Hawryluk, Joanna M. Tzingounis, Anastasios V. Mulkey, Daniel K. Moreira, Thiago S. Takakura, Ana C. |
| Author_xml | – sequence: 1 givenname: Daniel K. surname: Mulkey fullname: Mulkey, Daniel K. organization: University of Connecticut – sequence: 2 givenname: Virginia E. surname: Hawkins fullname: Hawkins, Virginia E. organization: University of Connecticut – sequence: 3 givenname: Joanna M. surname: Hawryluk fullname: Hawryluk, Joanna M. organization: University of Connecticut – sequence: 4 givenname: Ana C. surname: Takakura fullname: Takakura, Ana C. organization: University of São Paulo – sequence: 5 givenname: Thiago S. surname: Moreira fullname: Moreira, Thiago S. organization: University of São Paulo – sequence: 6 givenname: Anastasios V. surname: Tzingounis fullname: Tzingounis, Anastasios V. organization: University of Connecticut |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25603782$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3389_fnins_2020_615666 crossref_primary_10_1523_ENEURO_0404_18_2018 crossref_primary_10_1113_jphysiol_2014_287185 crossref_primary_10_1016_j_bbrep_2015_07_003 crossref_primary_10_1016_j_yebeh_2016_09_034 crossref_primary_10_3389_fneur_2023_1137182 crossref_primary_10_1113_JP276104 crossref_primary_10_1111_epi_13676 crossref_primary_10_1523_JNEUROSCI_2316_16_2016 |
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| Notes | which took place at the 1st PanAmerican Congress of Physiological Sciences, Iguassu Falls, Brazil on 3 August 2014. This review was presented at the symposium New advances in the neural control of breathing ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 ObjectType-Article-1 ObjectType-Feature-2 This review was presented at the symposium New advances in the neural control of breathing, which took place at the 1st PanAmerican Congress of Physiological Sciences, Iguassu Falls, Brazil on 3 August 2014. |
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| Snippet | Central chemoreception is the mechanism by which CO2/H+‐sensitive neurons (i.e. chemoreceptors) regulate breathing in response to changes in tissue CO2/H+.... Central chemoreception is the mechanism by which CO₂/H(+) -sensitive neurons (i.e. chemoreceptors) regulate breathing in response to changes in tissue CO₂/H(+)... Central chemoreception is the mechanism by which CO2/H+-sensitive neurons (i.e. chemoreceptors) regulate breathing in response to changes in tissue CO2/H+.... 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... |
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| SubjectTerms | Animals Brain Stem - cytology Brain Stem - metabolism Brain Stem - physiology Chemoreceptor Cells - metabolism Chemoreceptor Cells - physiology Epilepsy Humans KCNQ Potassium Channels - genetics KCNQ Potassium Channels - metabolism Medical research Respiration Symposium Section Reviews: New Advances in the Neural Control of Breathing |
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| Title | Molecular underpinnings of ventral surface chemoreceptor function: focus on KCNQ channels |
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