Mechanisms underlying hyperpolarization evoked by P2Y receptor activation in mouse distal colon

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Abstract

In murine colonic circular muscle, ATP mediates fast component of the nerve-evoked inhibitory junction potentials, via activation of P2Yreceptors and opening of apamin-sensitive Ca2+-dependent K+ channels. We investigated, using microelectrode recordings, the intracellular eventsfollowing P2Y-receptor activation by electrical field stimulation or by adenosine 5′-O-2-thiodiphosphate (ADPβS), ATP stable analogue. The fastinhibitoryjunction potential amplitude was reduced by thapsigargin or ciclopiazonic acid (CPA), sarcoplasmic reticulum Ca2+-ATPase inhibitors,by ryanodine, which inhibits Ca2+ release from ryanodine-sensitive stores, and by 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), anadenylyl cyclase inhibitor. Fast-inhibitory junction potentials were enhanced by 2-aminoethoxy-diphenylborate (2-APB), an IP3 receptor inhibitoror by {1-[6((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl]-1H-pyrrole-2,5-dione} (U-73122), a phospholipase C inhibitor. ADPβSinduced hyperpolarization that was significantly reduced by apamin, thapsigargin, CPA, ryanodine, 2-APB and SQ 22,536, but it was not modifiedby U-73122. Forskolin, an adenylyl cyclase activator, induced hyperpolarization that was inhibited by SQ 22,536, apamin or ryanodine. Inconclusion, in murine colon, apamin-sensitive hyperpolarization induced by activation of P2Y receptors is mainly mediated by release of Ca2+from intracellular ryanodine-dependent stores via a mechanism involving adenylyl cyclase.
Lingua originaleEnglish
pagine (da-a)174-180
Numero di pagine7
RivistaEuropean Journal of Pharmacology
Volume544
Stato di pubblicazionePublished - 2006

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Ryanodine
Apamin
Colon
Thapsigargin
Adenylyl Cyclases
Adenosine Triphosphate
Inositol 1,4,5-Trisphosphate Receptors
Acids
Calcium-Transporting ATPases
Sarcoplasmic Reticulum
Type C Phospholipases
Microelectrodes
Colforsin
Electric Stimulation
Muscles
9-(tetrahydro-2-furyl)-adenine
1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione

All Science Journal Classification (ASJC) codes

  • Pharmacology

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title = "Mechanisms underlying hyperpolarization evoked by P2Y receptor activation in mouse distal colon",
abstract = "In murine colonic circular muscle, ATP mediates fast component of the nerve-evoked inhibitory junction potentials, via activation of P2Yreceptors and opening of apamin-sensitive Ca2+-dependent K+ channels. We investigated, using microelectrode recordings, the intracellular eventsfollowing P2Y-receptor activation by electrical field stimulation or by adenosine 5′-O-2-thiodiphosphate (ADPβS), ATP stable analogue. The fastinhibitoryjunction potential amplitude was reduced by thapsigargin or ciclopiazonic acid (CPA), sarcoplasmic reticulum Ca2+-ATPase inhibitors,by ryanodine, which inhibits Ca2+ release from ryanodine-sensitive stores, and by 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), anadenylyl cyclase inhibitor. Fast-inhibitory junction potentials were enhanced by 2-aminoethoxy-diphenylborate (2-APB), an IP3 receptor inhibitoror by {1-[6((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl]-1H-pyrrole-2,5-dione} (U-73122), a phospholipase C inhibitor. ADPβSinduced hyperpolarization that was significantly reduced by apamin, thapsigargin, CPA, ryanodine, 2-APB and SQ 22,536, but it was not modifiedby U-73122. Forskolin, an adenylyl cyclase activator, induced hyperpolarization that was inhibited by SQ 22,536, apamin or ryanodine. Inconclusion, in murine colon, apamin-sensitive hyperpolarization induced by activation of P2Y receptors is mainly mediated by release of Ca2+from intracellular ryanodine-dependent stores via a mechanism involving adenylyl cyclase.",
author = "Zizzo, {Maria Grazia} and Serio, {Rosa Maria} and Flavia Mule'",
year = "2006",
language = "English",
volume = "544",
pages = "174--180",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
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TY - JOUR

T1 - Mechanisms underlying hyperpolarization evoked by P2Y receptor activation in mouse distal colon

AU - Zizzo, Maria Grazia

AU - Serio, Rosa Maria

AU - Mule', Flavia

PY - 2006

Y1 - 2006

N2 - In murine colonic circular muscle, ATP mediates fast component of the nerve-evoked inhibitory junction potentials, via activation of P2Yreceptors and opening of apamin-sensitive Ca2+-dependent K+ channels. We investigated, using microelectrode recordings, the intracellular eventsfollowing P2Y-receptor activation by electrical field stimulation or by adenosine 5′-O-2-thiodiphosphate (ADPβS), ATP stable analogue. The fastinhibitoryjunction potential amplitude was reduced by thapsigargin or ciclopiazonic acid (CPA), sarcoplasmic reticulum Ca2+-ATPase inhibitors,by ryanodine, which inhibits Ca2+ release from ryanodine-sensitive stores, and by 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), anadenylyl cyclase inhibitor. Fast-inhibitory junction potentials were enhanced by 2-aminoethoxy-diphenylborate (2-APB), an IP3 receptor inhibitoror by {1-[6((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl]-1H-pyrrole-2,5-dione} (U-73122), a phospholipase C inhibitor. ADPβSinduced hyperpolarization that was significantly reduced by apamin, thapsigargin, CPA, ryanodine, 2-APB and SQ 22,536, but it was not modifiedby U-73122. Forskolin, an adenylyl cyclase activator, induced hyperpolarization that was inhibited by SQ 22,536, apamin or ryanodine. Inconclusion, in murine colon, apamin-sensitive hyperpolarization induced by activation of P2Y receptors is mainly mediated by release of Ca2+from intracellular ryanodine-dependent stores via a mechanism involving adenylyl cyclase.

AB - In murine colonic circular muscle, ATP mediates fast component of the nerve-evoked inhibitory junction potentials, via activation of P2Yreceptors and opening of apamin-sensitive Ca2+-dependent K+ channels. We investigated, using microelectrode recordings, the intracellular eventsfollowing P2Y-receptor activation by electrical field stimulation or by adenosine 5′-O-2-thiodiphosphate (ADPβS), ATP stable analogue. The fastinhibitoryjunction potential amplitude was reduced by thapsigargin or ciclopiazonic acid (CPA), sarcoplasmic reticulum Ca2+-ATPase inhibitors,by ryanodine, which inhibits Ca2+ release from ryanodine-sensitive stores, and by 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), anadenylyl cyclase inhibitor. Fast-inhibitory junction potentials were enhanced by 2-aminoethoxy-diphenylborate (2-APB), an IP3 receptor inhibitoror by {1-[6((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl]-1H-pyrrole-2,5-dione} (U-73122), a phospholipase C inhibitor. ADPβSinduced hyperpolarization that was significantly reduced by apamin, thapsigargin, CPA, ryanodine, 2-APB and SQ 22,536, but it was not modifiedby U-73122. Forskolin, an adenylyl cyclase activator, induced hyperpolarization that was inhibited by SQ 22,536, apamin or ryanodine. Inconclusion, in murine colon, apamin-sensitive hyperpolarization induced by activation of P2Y receptors is mainly mediated by release of Ca2+from intracellular ryanodine-dependent stores via a mechanism involving adenylyl cyclase.

UR - http://hdl.handle.net/10447/28753

M3 - Article

VL - 544

SP - 174

EP - 180

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

ER -