TASK-like potassium channels and oxygen sensing in the carotid body.
Chemosensing by type-1 cells of the carotid body involves a series of events which culminate in the calcium-dependent secretion of neurotransmitter substances which then excite afferent nerves. This response is mediated via membrane depolarisation and voltage-gated calcium entry. Studies utilising i...
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| Format: | Journal article |
| Language: | English |
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2007
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| _version_ | 1797063421669146624 |
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| author | Buckler, K |
| author_facet | Buckler, K |
| author_sort | Buckler, K |
| collection | OXFORD |
| description | Chemosensing by type-1 cells of the carotid body involves a series of events which culminate in the calcium-dependent secretion of neurotransmitter substances which then excite afferent nerves. This response is mediated via membrane depolarisation and voltage-gated calcium entry. Studies utilising isolated cells indicates that the membrane depolarisation in response to hypoxia, and acidosis, appears to be primarily mediated via the inhibition of a background K(+)-current. The pharmacological and biophysical characteristics of these channels suggest that they are probably closely related to the TASK subfamily of tandem-P-domain K(+)-channels. Indeed they show greatest similarity to TASK-1 and -3. In addition to being sensitive to hypoxia and acidosis, the background K(+)-channels of the type-1 cell are also remarkably sensitive to inhibition of mitochondrial energy metabolism. Metabolic poisons are known potent stimulants of the carotid body and cause membrane depolarisation of type-1 cells. In the presence of metabolic inhibitors hypoxic sensitivity is lost suggesting that oxygen sensing may itself be mediated via depression of mitochondrial energy production. Thus these TASK-like background channels play a central role in mediating the chemotransduction of several different stimuli within the type-1 cell. The mechanisms by which metabolic/oxygen sensitivity might be conferred upon these channels are briefly discussed. |
| first_indexed | 2024-03-06T20:59:37Z |
| format | Journal article |
| id | oxford-uuid:3a70af6a-7fcb-4e46-b462-31a5051220ed |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T20:59:37Z |
| publishDate | 2007 |
| record_format | dspace |
| spelling | oxford-uuid:3a70af6a-7fcb-4e46-b462-31a5051220ed2022-03-26T14:01:33ZTASK-like potassium channels and oxygen sensing in the carotid body.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:3a70af6a-7fcb-4e46-b462-31a5051220edEnglishSymplectic Elements at Oxford2007Buckler, KChemosensing by type-1 cells of the carotid body involves a series of events which culminate in the calcium-dependent secretion of neurotransmitter substances which then excite afferent nerves. This response is mediated via membrane depolarisation and voltage-gated calcium entry. Studies utilising isolated cells indicates that the membrane depolarisation in response to hypoxia, and acidosis, appears to be primarily mediated via the inhibition of a background K(+)-current. The pharmacological and biophysical characteristics of these channels suggest that they are probably closely related to the TASK subfamily of tandem-P-domain K(+)-channels. Indeed they show greatest similarity to TASK-1 and -3. In addition to being sensitive to hypoxia and acidosis, the background K(+)-channels of the type-1 cell are also remarkably sensitive to inhibition of mitochondrial energy metabolism. Metabolic poisons are known potent stimulants of the carotid body and cause membrane depolarisation of type-1 cells. In the presence of metabolic inhibitors hypoxic sensitivity is lost suggesting that oxygen sensing may itself be mediated via depression of mitochondrial energy production. Thus these TASK-like background channels play a central role in mediating the chemotransduction of several different stimuli within the type-1 cell. The mechanisms by which metabolic/oxygen sensitivity might be conferred upon these channels are briefly discussed. |
| spellingShingle | Buckler, K TASK-like potassium channels and oxygen sensing in the carotid body. |
| title | TASK-like potassium channels and oxygen sensing in the carotid body. |
| title_full | TASK-like potassium channels and oxygen sensing in the carotid body. |
| title_fullStr | TASK-like potassium channels and oxygen sensing in the carotid body. |
| title_full_unstemmed | TASK-like potassium channels and oxygen sensing in the carotid body. |
| title_short | TASK-like potassium channels and oxygen sensing in the carotid body. |
| title_sort | task like potassium channels and oxygen sensing in the carotid body |
| work_keys_str_mv | AT bucklerk tasklikepotassiumchannelsandoxygensensinginthecarotidbody |