ATP Receptor-Operated Ca2+ Influx and Catecholamine Release From Neuronal Cells

Inoue, Katsue; Nakazawa, Kenichi

doi:10.1152/physiologyonline.1992.7.2.56

Cited by 16 publications

(20 citation statements)

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“…recorded from circular muscle of the guinea-pig fundus is also generated by stimulation of NANC nerves, and this potential can be blocked by apamin (Komori & Suzuki, 1986) or suramin (Ohno et al, 1993). Apamin is an inhibitor of Ca2+-activated K+-channels (Romey & Lazdunski, 1984), while suramin is an inhibitor of the ATP-receptor (Inoue & Nakazawa, 1992). Therefore, the NANC ij.p.…”

Section: Discussionmentioning

confidence: 99%

Properties of the inhibitory junction potential in smooth muscle of the guinea‐pig gastric fundus

Ohno

Lü

Yamamoto

et al. 1996

British J Pharmacology

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1 In circular smooth muscle of the guinea-pig gastric fundus, transmural nerve stimulation evoked a cholinergic excitatory junction potential (ej.p.), and blockade of the ej.p. by atropine revealed a nonadrenergic non-cholinergic (NANC) inhibitory junction potential (ij.p.).2 The amplitude of the ej.p. was increased by apamin, suramin or NGnitro-L-arginine (L-NOARG), with no significant change in the membrane potential. 3 The ij.p. consisted of two components (fast and slow); apamin inhibited the former, nitroarginine inhibited the latter, and suramin inhibited both components. 4 Apamin inhibited the hyperpolarization produced by adenosine 5'-triphosphate (ATP) but not by vasoactive intestinal polypeptide (VIP). Suramin inhibited the hyperpolarization produced by VIP but not by ATP. The sodium nitroprusside (SNP)-induced hyperpolarization was not blocked by apamin or suramin. L-NOARG or tetrodotoxin did not inhibit the hyperpolarization produced by ATP, VIP or SNP. 5 The data did not support the hypothesis that ATP, VIP or nitric oxide (NO) is the main transmitter responsible for generation of the NANC ij.p. in the fundus. 6 Actions of L-NOARG suggest that endogenous NO may be involved in junctional transmission, mainly as an inhibitory modulator of cholinergic transmission.

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Section: Discussionmentioning

confidence: 99%

Properties of the inhibitory junction potential in smooth muscle of the guinea‐pig gastric fundus

Ohno

Lü

Yamamoto

et al. 1996

British J Pharmacology

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“…However, low-affinity electrostatic binding of TNP-ATP to phospholipids has been reported to be minimal (Moezydlowski and Fortes, 1981). We were also precluded from using reactive blue 2, an alternative P, receptor blocker (Inoue and Nakazawa, 1992) to quench the P, receptor component of ATP binding sites because it exhibited considerable intrinsic fluorescence, in the micromolar concentration range, over the wavelengths used for detection of TNP-ATP binding. The significant block of the stereocilia TNP-ATP binding (57%) by suramin is highly suggestive of specific binding of the TNP-ATP to P, purinoceptors localized to this region.…”

Section: Discussionmentioning

confidence: 99%

Fluorescence imaging of extracellular purinergic receptor sites and putative ecto-ATPase sites on isolated cochlear hair cells

1994

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Fluorescence imaging of extracellular adenosine-5′-triphosphate (ATP) binding sites on inner and outer hair cells isolated from the guinea pig organ of Corti was achieved using the fluorescent analog of ATP, 2′- (or-3′)-O-(trinitrophenyl)adenosine-5′- triphosphate (TNP-ATP; 30–75 microM). This analog, which fluoresces on binding to these sites, was pressure applied by micropipette while hair cells were viewed by fluorescence microscopy. Fluorescence imaging revealed a widespread distribution of extracellular binding sites, including the stereocilia, cuticular plate, and the basolateral margins of the cells, but particularly in infracuticular and infranuclear regions. In support of extracellular binding, simultaneous electrophysiological recordings demonstrated that rapid washout of TNP-ATP-induced fluorescence was dependent upon cell integrity. Suramin, a nonselective P2 purinoceptor antagonist, coapplied with TNP-ATP, reduced the fluorescence observed on the stereocilia and apical surface of the cuticular plate only. This implies that binding sites on the apical surface of hair cells are P2 receptors, consistent with previous electrophysiological evidence for localization of P2 receptors to the apical surface of cochlear hair cells (Housley et al., 1992). Binding of TNP-ATP to P2 purinoceptors was confirmed by its antagonism of the inward current elicited by ATP (10 microM) in voltage-clamped hair cells. Fluorescence from the basolateral margin was significantly quenched when TNP-ATP was applied in divalent cation-free solution. Because divalent cations are required for ATPase activity, this finding provides evidence for the presence of ecto-ATPases on the basolateral membrane of hair cells. The divalent cation-free condition had no significant effect on the ATP-gated P2 purinoceptor conductance. We propose that there are two classes of ATP binding sites on cochlear hair cells: apically located P2 purinoceptors gating nonselective cation channels and basolaterally located ecto- ATPases that may be involved in purine turnover.

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“…These findings suggest a role for able to depolarize cell membranes and thereby activate voltage-dependent Ca2 channels, Nakazavva and Inoue [3,4,8] have suggested that ATP-induced Ca2 intlux through these chan nels does not contribute to the regulation of [Ca2 ], in PC12 cells. They reasoned that Ca2 -dependent inactivation of Ca2 channels during the ATP-activated cation-selective current un derlies the lack of contribution of the voltagedependent Ca2 channels in the regulation of [Ca2'],.…”

Section: Introductionmentioning

confidence: 84%

“…ATP seems to act on these cells by binding to P:-purinergic receptors [3], During exposure of the cells to ATP the membrane potential is depolarized, even in the absence of extracellular Ca2 , due to activation of a large inward current mainly car ried by Na ions [5]. The depolarization in duced by 100 pA/ ATP reached near 0 mV [8J.…”

Section: Discussionmentioning

confidence: 99%

“…ATP excites a subpopulation of rat dorsal root neurons [1] and rat sensory neurons [2], It induces nonselective cation currents, depolar izes the cell membrane and induces catechola mine release in rat pheochromocytoma (PC12) cells [3][4][5]. These findings suggest a role for able to depolarize cell membranes and thereby activate voltage-dependent Ca2 channels, Nakazavva and Inoue [3,4,8] have suggested that ATP-induced Ca2 intlux through these chan nels does not contribute to the regulation of [Ca2 ], in PC12 cells.…”

Section: Introductionmentioning

confidence: 99%

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Multiple Pathways for ATP-lnduced Intracellular Calcium Elevation in Pheochromocytoma (PC12) Cells

Gollasch¹,

Haller²

1995

Kidney Blood Press Res

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Extracellular ATP excites neurons in both the peripheral and central nervous system. To elucidate the mechanisms involved, we used spectrofluorometric analysis to study the pathways by which extracellular ATP elevates the intracellular Ca²⁺ concentration ([Ca²⁺]_i) in individual, fura-2-loaded, rat pheochromocytoma PC12 cells. ATP ( > 1 µM) increased [Ca²⁺]_i. The ATP effect on [Ca²⁺]_i was completely abolished by a nominally Ca²⁺-free extracellular medium, which indicates that the ATP-induced increase in [Ca²⁺]i was due to an influx of extracellular Ca²⁺. We next applied specific blockers of voltage-dependent Ca²⁺ channels and used experimental protocols with depolarizing external K⁺-rich solutions. Our results show that ATP induces influx of extracellular Ca²⁺ through (a) dihydropyridine-sensitive (L_n-type) Ca²⁺ channels, (b) Ca²⁺-permeable, voltage-independent, Cd²⁺-insensitive cation channels, and (c) an as yet unidentified, voltage-dependent, Cd²⁺-sensitive Ca²⁺ influx system.

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ATP Receptor-Operated Ca2+ Influx and Catecholamine Release From Neuronal Cells

Abstract: The physiological function of extracellular ATP was investigated using PC-12 cells as a model neuronal cell. The mechanism of action of ATP proposed is that ATP stimulates P2-purinoceptors, activates Ca2+-permeable cation channels, and causes Ca2+ influx, triggering catecholamine release.

Cited by 16 publications

References 0 publications

Properties of the inhibitory junction potential in smooth muscle of the guinea‐pig gastric fundus

Properties of the inhibitory junction potential in smooth muscle of the guinea‐pig gastric fundus

Fluorescence imaging of extracellular purinergic receptor sites and putative ecto-ATPase sites on isolated cochlear hair cells

Multiple Pathways for ATP-lnduced Intracellular Calcium Elevation in Pheochromocytoma (PC12) Cells

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