Cholecystokinin-8 induces intracellular calcium signaling in cultured myenteric neurons from neonatal guinea pigs

Weizhen Zhang; Bradley J. Segura; Michael W. Mulholland

doi:10.1016/S0196-9781(02)00136-5

Cholecystokinin-8 induces intracellular calcium signaling in cultured myenteric neurons from neonatal guinea pigs

Weizhen Zhang, Bradley J. Segura, Michael W. Mulholland

Research output: Contribution to journal › Article › peer-review

17 Scopus citations

Abstract

The responsiveness of cultured myenteric neurons to cholecystokinin (CCK-8) was examined using fura-2-based digital microfluorimetric measurement of intracellular calcium ([Ca²⁺]_i). CCK-8 (10^-10-10^-6M) evoked concentration-dependent increases in percentage of neurons responding (8-52%) and Δ[Ca²⁺]_i (76-169nM). Gastrin (1μM) also induced an increase in [Ca²⁺]_i in 29±6% of neurons (Δ[Ca²⁺]_i: 71±3nM). L-364,718, an antagonist for the CCK-A receptor, blocked [Ca²⁺]_i response to CCK-8. Removal of extracellular calcium eliminated CCK-induced [Ca²⁺]_i increments, as did the addition of the calcium channel inhibitors nickel (1mM) and lanthanum (5mM). Nifedipine (1-50μM) dose-dependently attenuated CCK-caused [Ca²⁺]_i responses. CCK evokes [Ca²⁺]_i signaling in myenteric neurons by the influx of extracellular calcium, likely through L-type calcium channels.

Original language	English (US)
Pages (from-to)	1793-1801
Number of pages	9
Journal	Peptides
Volume	23
Issue number	10
DOIs	https://doi.org/10.1016/S0196-9781(02)00136-5
State	Published - Oct 1 2002
Externally published	Yes

Bibliographical note

Funding Information:
This study was supported by NIH grant DK43225.

Keywords

Calcium channel
Enteric nervous system
Fura-2 acetoxymethyl ester
Myenteric plexus
Signal transduction

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10.1016/S0196-9781(02)00136-5

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title = "Cholecystokinin-8 induces intracellular calcium signaling in cultured myenteric neurons from neonatal guinea pigs",

abstract = "The responsiveness of cultured myenteric neurons to cholecystokinin (CCK-8) was examined using fura-2-based digital microfluorimetric measurement of intracellular calcium ([Ca2+]i). CCK-8 (10-10-10-6M) evoked concentration-dependent increases in percentage of neurons responding (8-52%) and Δ[Ca2+]i (76-169nM). Gastrin (1μM) also induced an increase in [Ca2+]i in 29±6% of neurons (Δ[Ca2+]i: 71±3nM). L-364,718, an antagonist for the CCK-A receptor, blocked [Ca2+]i response to CCK-8. Removal of extracellular calcium eliminated CCK-induced [Ca2+]i increments, as did the addition of the calcium channel inhibitors nickel (1mM) and lanthanum (5mM). Nifedipine (1-50μM) dose-dependently attenuated CCK-caused [Ca2+]i responses. CCK evokes [Ca2+]i signaling in myenteric neurons by the influx of extracellular calcium, likely through L-type calcium channels.",

keywords = "Calcium channel, Enteric nervous system, Fura-2 acetoxymethyl ester, Myenteric plexus, Signal transduction",

author = "Weizhen Zhang and Segura, {Bradley J.} and Mulholland, {Michael W.}",

note = "Funding Information: This study was supported by NIH grant DK43225. ",

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T1 - Cholecystokinin-8 induces intracellular calcium signaling in cultured myenteric neurons from neonatal guinea pigs

AU - Zhang, Weizhen

AU - Segura, Bradley J.

AU - Mulholland, Michael W.

N1 - Funding Information: This study was supported by NIH grant DK43225.

PY - 2002/10/1

Y1 - 2002/10/1

N2 - The responsiveness of cultured myenteric neurons to cholecystokinin (CCK-8) was examined using fura-2-based digital microfluorimetric measurement of intracellular calcium ([Ca2+]i). CCK-8 (10-10-10-6M) evoked concentration-dependent increases in percentage of neurons responding (8-52%) and Δ[Ca2+]i (76-169nM). Gastrin (1μM) also induced an increase in [Ca2+]i in 29±6% of neurons (Δ[Ca2+]i: 71±3nM). L-364,718, an antagonist for the CCK-A receptor, blocked [Ca2+]i response to CCK-8. Removal of extracellular calcium eliminated CCK-induced [Ca2+]i increments, as did the addition of the calcium channel inhibitors nickel (1mM) and lanthanum (5mM). Nifedipine (1-50μM) dose-dependently attenuated CCK-caused [Ca2+]i responses. CCK evokes [Ca2+]i signaling in myenteric neurons by the influx of extracellular calcium, likely through L-type calcium channels.

AB - The responsiveness of cultured myenteric neurons to cholecystokinin (CCK-8) was examined using fura-2-based digital microfluorimetric measurement of intracellular calcium ([Ca2+]i). CCK-8 (10-10-10-6M) evoked concentration-dependent increases in percentage of neurons responding (8-52%) and Δ[Ca2+]i (76-169nM). Gastrin (1μM) also induced an increase in [Ca2+]i in 29±6% of neurons (Δ[Ca2+]i: 71±3nM). L-364,718, an antagonist for the CCK-A receptor, blocked [Ca2+]i response to CCK-8. Removal of extracellular calcium eliminated CCK-induced [Ca2+]i increments, as did the addition of the calcium channel inhibitors nickel (1mM) and lanthanum (5mM). Nifedipine (1-50μM) dose-dependently attenuated CCK-caused [Ca2+]i responses. CCK evokes [Ca2+]i signaling in myenteric neurons by the influx of extracellular calcium, likely through L-type calcium channels.

KW - Calcium channel

KW - Enteric nervous system

KW - Fura-2 acetoxymethyl ester

KW - Myenteric plexus

KW - Signal transduction

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Cholecystokinin-8 induces intracellular calcium signaling in cultured myenteric neurons from neonatal guinea pigs

Abstract

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