{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,16]],"date-time":"2026-05-16T04:31:00Z","timestamp":1778905860825,"version":"3.51.4"},"reference-count":40,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2009,1,14]],"date-time":"2009-01-14T00:00:00Z","timestamp":1231891200000},"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":[[2009,1,15]]},"abstract":"<jats:p>GABA is expressed in carotid body (CB) chemoreceptor type I cells and has previously been reported to modulate sensory transmission via presynaptic GABA<jats:sub>B<\/jats:sub> receptors. Because low doses of clinically important GABA<jats:sub>A<\/jats:sub> receptor (GABA<jats:sub>A<\/jats:sub>R) agonists, e.g. benzodiazepines, have been reported to depress afferent CB responses to hypoxia, we investigated the potential contribution of GABA<jats:sub>A<\/jats:sub>R in co\u2010cultures of rat type I cells and sensory petrosal neurones (PNs). During gramicidin perforated\u2010patch recordings (to preserve intracellular Cl<jats:sup>\u2212<\/jats:sup>), GABA and\/or the GABA<jats:sub>A<\/jats:sub> agonist muscimol (50 \u03bc<jats:sc>m<\/jats:sc>) induced a bicuculline\u2010sensitive membrane depolarization in isolated PNs. GABA\u2010induced whole\u2010cell currents reversed at \u223c\u221238 mV and had an EC<jats:sub>50<\/jats:sub> of \u223c10 \u03bc<jats:sc>m<\/jats:sc> (Hill coefficient =\u223c1) at \u221260 mV. During simultaneous PN and type I cell recordings at functional chemosensory units in co\u2010culture, bicuculline reversibly potentiated the PN, but not type I cell, depolarizing response to hypoxia. Application of the CB excitatory neurotransmitter ATP (1 \u03bc<jats:sc>m<\/jats:sc>) over the soma of functional PN induced a spike discharge that was markedly suppressed during co\u2010application with GABA (2 \u03bc<jats:sc>m<\/jats:sc>), even though GABA alone was excitatory. RT\u2010PCR analysis detected expression of GABAergic markers including mRNA for \u03b11, \u03b12, \u03b22, \u03b32S, \u03b32L and \u03b33 GABA<jats:sub>A<\/jats:sub>R subunits in petrosal ganglia extracts. Also, CB extracts contained mRNAs for GABA biosynthetic markers, i.e. glutamate decarboxylase (GAD) isoforms GAD 67A,E, and GABA transporter isoforms GAT 2,3 and BGT\u20101. In CB sections, sensory nerve endings apposed to type I cells were immunopositive for the GABA<jats:sub>A<\/jats:sub>R \u03b2 subunit. These data suggest that GABA, released from the CB during hypoxia, inhibits sensory discharge postsynaptically via a shunting mechanism involving GABA<jats:sub>A<\/jats:sub> receptors.<\/jats:p>","DOI":"10.1113\/jphysiol.2008.165035","type":"journal-article","created":{"date-parts":[[2008,11,25]],"date-time":"2008-11-25T01:34:29Z","timestamp":1227576869000},"page":"329-344","source":"Crossref","is-referenced-by-count":32,"title":["Postsynaptic action of GABA in modulating sensory transmission in co\u2010cultures of rat carotid body via GABA<sub>A<\/sub> 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