Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.

Cholecystokinin (CCK) facilitates the process of satiation via activation of vagal afferent neurons innervating the upper gastrointestinal tract. Recent findings indicate CCK acts on these neurons via a ruthenium red (RuR) sensitive pathway that involves members of the vanilloid (V) subfamily of tra...

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Autores principales:	Dallas C Kinch, James H Peters, Steven M Simasko
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/33b16dc9148c46ab81b33963b378ed8e
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spelling	oai:doaj.org-article:33b16dc9148c46ab81b33963b378ed8e2021-11-18T07:22:16ZComparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.1932-620310.1371/journal.pone.0034755https://doaj.org/article/33b16dc9148c46ab81b33963b378ed8e2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22514663/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Cholecystokinin (CCK) facilitates the process of satiation via activation of vagal afferent neurons innervating the upper gastrointestinal tract. Recent findings indicate CCK acts on these neurons via a ruthenium red (RuR) sensitive pathway that involves members of the vanilloid (V) subfamily of transient receptor potential (TRP) channels. To further test this mechanism, the mouse provides an ideal model in which genetic tools could be applied. However, whether CCK acts by similar mechanism(s) in mice has not been determined. In the present study we explored the actions of CCK on nodose neurons isolated from Sprague Dawley (SD) rat and two strains of mice; C57BL/6 and BalbC using fluorescence-based calcium imaging. With minor exceptions nodose neurons isolated from all species/strains behaved similarly. They all respond to brief depolarization with a large calcium transient. A significant subset of neurons responded to capsaicin (CAP), a TRPV1 agonist, although neurons from C57BL/6 were 10-fold more sensitive to CAP than SD rats or BalbC mice, and a significantly smaller fraction of neurons from BalbC mice responded to CAP. CCK-8 dose-dependently activated a subpopulation of neurons with similar dose dependency, percent responders, and overlap between CCK and CAP responsiveness. In all species/strains CCK-8 induced activation was significantly attenuated (but not completely blocked) by pretreatment with the TRPV channel blocker RuR. Surprisingly, the CCK analogue JMV-180, which is reported to have pure antagonistic properties in rat but mixed agonist/antagonist properties in mice, behaved as a pure antagonist to CCK in both rat and mouse neurons. The pure antagonistic action of JMV-180 in this in vitro preparation suggests that prior reported differential effects of JMV-180 on satiation in rats versus mouse must be mediated by a site other than vagal afferent activation.Dallas C KinchJames H PetersSteven M SimaskoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 4, p e34755 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Dallas C Kinch James H Peters Steven M Simasko Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.
description	Cholecystokinin (CCK) facilitates the process of satiation via activation of vagal afferent neurons innervating the upper gastrointestinal tract. Recent findings indicate CCK acts on these neurons via a ruthenium red (RuR) sensitive pathway that involves members of the vanilloid (V) subfamily of transient receptor potential (TRP) channels. To further test this mechanism, the mouse provides an ideal model in which genetic tools could be applied. However, whether CCK acts by similar mechanism(s) in mice has not been determined. In the present study we explored the actions of CCK on nodose neurons isolated from Sprague Dawley (SD) rat and two strains of mice; C57BL/6 and BalbC using fluorescence-based calcium imaging. With minor exceptions nodose neurons isolated from all species/strains behaved similarly. They all respond to brief depolarization with a large calcium transient. A significant subset of neurons responded to capsaicin (CAP), a TRPV1 agonist, although neurons from C57BL/6 were 10-fold more sensitive to CAP than SD rats or BalbC mice, and a significantly smaller fraction of neurons from BalbC mice responded to CAP. CCK-8 dose-dependently activated a subpopulation of neurons with similar dose dependency, percent responders, and overlap between CCK and CAP responsiveness. In all species/strains CCK-8 induced activation was significantly attenuated (but not completely blocked) by pretreatment with the TRPV channel blocker RuR. Surprisingly, the CCK analogue JMV-180, which is reported to have pure antagonistic properties in rat but mixed agonist/antagonist properties in mice, behaved as a pure antagonist to CCK in both rat and mouse neurons. The pure antagonistic action of JMV-180 in this in vitro preparation suggests that prior reported differential effects of JMV-180 on satiation in rats versus mouse must be mediated by a site other than vagal afferent activation.
format	article
author	Dallas C Kinch James H Peters Steven M Simasko
author_facet	Dallas C Kinch James H Peters Steven M Simasko
author_sort	Dallas C Kinch
title	Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.
title_short	Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.
title_full	Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.
title_fullStr	Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.
title_full_unstemmed	Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.
title_sort	comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/33b16dc9148c46ab81b33963b378ed8e
work_keys_str_mv	AT dallasckinch comparativepharmacologyofcholecystokinininducedactivationofculturedvagalafferentneuronsfromratsandmice AT jameshpeters comparativepharmacologyofcholecystokinininducedactivationofculturedvagalafferentneuronsfromratsandmice AT stevenmsimasko comparativepharmacologyofcholecystokinininducedactivationofculturedvagalafferentneuronsfromratsandmice
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Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.

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