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• W2095893583 abstract "The neurotransmitter mechanisms that process acid hypercapnia in the mammalian carotid body (CB) are poorly understood. Using a co-culture model containing rat CB chemoreceptor (type 1 cell) clusters and petrosal neurons (PN), we tested the hypothesis that co-released ACh and ATP was an important mechanism. Sensory transmission from type I clusters to PN in co-culture occurred at chemical synapses via co-release of ATP and ACh because isohydric hypercapnia depolarized and/or increased firing in co-cultured PN, but not in PN cultured alone; PN chemoexcitatory responses were inhibited by decreasing the extracellular Ca 2+ : Mg 2+ ratio; partial inhibition of these responses occurred during separate perfusion of cholinergic (hexamethonium or mecamylamine) and P2X (suramin) receptor blockers, although inhibition was often complete with both blockers present; and rapid chemoexcitatory responses to hypercapnia were inhibited by acetazolamide (10 μM), an inhibitor of carbonic anhydrase, localized in type I cells. Acidosis (pH = 7.0, 7.2) enhanced the ATP-induced whole cell current in functional PN relative to that at physiologic pH (7.4), suggesting that increased sensitivity of postsynaptic P2X receptors may contribute to acid chemotransmission. Type I cells in CB tissue sections expressed vesicular acetylcholine transporter (VAChT), a cholinergic marker, as revealed by confocal immunofluorescence. Thus co-release of ACh and ATP is an important neurotransmitter mechanism for processing isohydric and acidic hypercapnia in the rat carotid body." @default.
• W2095893583 created "2016-06-24" @default.
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• W2095893583 date "2004-12-01" @default.
• W2095893583 modified "2023-09-25" @default.
• W2095893583 title "CO₂/pH Chemosensory Signaling in Co-Cultures of Rat Carotid Body Receptors and Petrosal Neurons: Role of ATP and ACh" @default.
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• W2095893583 doi "https://doi.org/10.1152/jn.01099.2003" @default.
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