The Journal of Neuroscience, September 13, 2006, ():
Expression of Multiple P2X Receptors by Glossopharyngeal Neurons Projecting to Rat Carotid Body O2-Chemoreceptors: Role in Nitric Oxide-Mediated Efferent Inhibition
J. Neurosci. Campanucci et al.
26: 9482
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Figure 14 legend: Working model for the role of GPN neurons in efferent inhibition of the rat CB via their activation by hypoxia and ATP. A reduction in arterial PO2 causes: (1) Inhibition of background (TASK1-like) and large-conductance Ca2+ activated (BK) K+ channels in type I cells, leading to depolarization, Ca2+ influx and neurotransmitter (ACh and ATP) release. These neurotransmitters act on petrosal sensory nerve endings via P2X receptors (P2XR) and nicotinic ACh receptors (nAChR) and initiate compensatory hyperventilation leading to restoration of blood PO2. (2) ATP may act on P2XR on nearby GPN nerve terminals, leading to Ca2+ influx via P2XR and/or depolarization-induced opening of voltage-gated Ca2+ channels. The rise in intracellular Ca2+ activates neuronal NOS (nNOS) leading to NO synthesis and release. NO action results in hyperpolarization of type I cells probably via activation of K+ channels (see Silva and Lewis, 2002), leading to reduction in neurotransmitter release. The latter may also result from NO-induced inhibition of L-type Ca2+ channels (Summers et al., 1999). (3) Hypoxia may also cause release of ATP from red blood cells (RBC; Ellsworth, 2000), which in turn may act on purinergic P2Y receptors on the endothelial cells, leading to activation of eNOS and release of NO. This new available source of ATP may diffuse through fenestrated capillaries (permeable to Evan’s blue dye) and excite paraganglion (GPN) neurons, thereby activating the efferent pathway (see 2). (4) Finally, hypoxia may also cause direct activation of GPN neurons by inhibiting background K+ channels (Campanucci et al., 2003), leading to depolarization and/or an increase in firing frequency. The resulting entry of extracellular Ca2+ via various voltage-dependent Ca2+ channels leads to nNOS activation, followed by NO synthesis and release.
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Figure 15 legend: Effect of the selective neuronal NOS inhibitor L-NAME on the BzATP-induced hyperpolarization in a type I cell co-cultured with GPN neurons. L-NAME (500 μM) caused a time-dependent reduction of this BzATP-induced hyperpolarization, which was likely mediated via NO release from activated adjacent GPN neurons (n = 3).
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Figure 16 legend: GPN paraganglia staining after perfusion with Evans blue dye. In A, localized dye staining (arrow) occurred in the area where proximal GPN neurons are concentrated. Also note strong dye staining in carotid body (CB) tissue. B, Localized dye staining in the area (boxed) where the distal population of GPN neurons are concentrated. C, Higher magnification of the boxed area marked in B, showing blood vessel staining and dye deposit in the surrounding tissue. Scale bars represent 100 μm (A-B) and 10 μm (C).
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