{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,16]],"date-time":"2026-05-16T04:30:49Z","timestamp":1778905849580,"version":"3.51.4"},"reference-count":60,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2003,11,1]],"date-time":"2003-11-01T00:00:00Z","timestamp":1067644800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2003,11]]},"abstract":"<jats:p>Background K<jats:sup>+<\/jats:sup> channels exert control over neuronal excitability by regulating resting potential and input resistance. Here, we show that GABA<jats:sub>B<\/jats:sub> receptor\u2010mediated activation of a background K<jats:sup>+<\/jats:sup> conductance modulates transmission at rat carotid body chemosensory synapses <jats:italic>in vitro<\/jats:italic>. Carotid body chemoreceptor (type I) cells expressed GABA<jats:sub>B(1)<\/jats:sub> and GABA<jats:sub>B(2)<\/jats:sub> subunits as well as endogenous GABA. The GABA<jats:sub>B<\/jats:sub> receptor agonist baclofen activated an anandamide\u2010 and Ba<jats:sup>2+<\/jats:sup>\u2010sensitive TASK\u20101\u2010like background K<jats:sup>+<\/jats:sup> conductance in chemoreceptor cell clusters, but was without effect on voltage\u2010gated Ca<jats:sup>2+<\/jats:sup> channels. Hydroxysaclofen (50 \u03bc<jats:sc>m<\/jats:sc>), 5\u2010aminovaleric acid (100 \u03bc<jats:sc>m<\/jats:sc>) and CGP 55845 (100 n<jats:sc>m<\/jats:sc>), selective GABA<jats:sub>B<\/jats:sub> receptor blockers, potentiated the hypoxia\u2010induced receptor potential; this effect was abolished by pre\u2010treatment with pertussis toxin (PTX; 500 ng ml<jats:sup>\u20101<\/jats:sup>), an inhibitor of G<jats:sub>i<\/jats:sub>, or by H\u201089 (50 \u03bc<jats:sc>m<\/jats:sc>), a selective inhibitor of protein kinase A. The protein kinase C inhibitor chelerythrine chloride (100 \u03bc<jats:sc>m<\/jats:sc>) was without effect on this potentiation. GABA<jats:sub>B<\/jats:sub> receptor blockers also caused depolarisation of type I cells in clusters, and enhanced spike discharge in spontaneously firing cells. In functional co\u2010cultures of type I clusters and petrosal sensory neurones, GABA<jats:sub>B<\/jats:sub> receptor blockers potentiated hypoxia\u2010induced postsynaptic chemosensory responses mediated by the fast\u2010acting transmitters ACh and ATP. Thus GABA<jats:sub>B<\/jats:sub> receptor\u2010mediated activation of TASK\u20101 or a related channel provides a presynaptic autoregulatory feedback mechanism that modulates fast synaptic transmission in the rat carotid body.<\/jats:p>","DOI":"10.1113\/jphysiol.2003.048298","type":"journal-article","created":{"date-parts":[[2003,9,2]],"date-time":"2003-09-02T00:52:06Z","timestamp":1062463926000},"page":"83-94","source":"Crossref","is-referenced-by-count":53,"title":["GABA Mediates Autoreceptor Feedback Inhibition in the Rat Carotid Body Via Presynaptic GABA<sub>B<\/sub> Receptors and TASK\u20101"],"prefix":"10.1113","volume":"553","author":[{"given":"Ian 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