Expression of cannabinoid CB1 receptors by vagal afferent neurons: Kinetics and role in influencing neurochemical phenotypeCitation formats

  • Authors:
  • Galina Burdyga
  • Andrea Varro
  • Rod Dimaline
  • David G. Thompson
  • Graham J. Dockray

Standard

Expression of cannabinoid CB1 receptors by vagal afferent neurons: Kinetics and role in influencing neurochemical phenotype. / Burdyga, Galina; Varro, Andrea; Dimaline, Rod; Thompson, David G.; Dockray, Graham J.

In: AJP: Gastrointestinal and Liver Physiology, Vol. 299, No. 1, 07.2010, p. G63-G69.

Research output: Contribution to journalArticle

Harvard

Burdyga, G, Varro, A, Dimaline, R, Thompson, DG & Dockray, GJ 2010, 'Expression of cannabinoid CB1 receptors by vagal afferent neurons: Kinetics and role in influencing neurochemical phenotype', AJP: Gastrointestinal and Liver Physiology, vol. 299, no. 1, pp. G63-G69. https://doi.org/10.1152/ajpgi.00059.2010

APA

Burdyga, G., Varro, A., Dimaline, R., Thompson, D. G., & Dockray, G. J. (2010). Expression of cannabinoid CB1 receptors by vagal afferent neurons: Kinetics and role in influencing neurochemical phenotype. AJP: Gastrointestinal and Liver Physiology, 299(1), G63-G69. https://doi.org/10.1152/ajpgi.00059.2010

Vancouver

Burdyga G, Varro A, Dimaline R, Thompson DG, Dockray GJ. Expression of cannabinoid CB1 receptors by vagal afferent neurons: Kinetics and role in influencing neurochemical phenotype. AJP: Gastrointestinal and Liver Physiology. 2010 Jul;299(1):G63-G69. https://doi.org/10.1152/ajpgi.00059.2010

Author

Burdyga, Galina ; Varro, Andrea ; Dimaline, Rod ; Thompson, David G. ; Dockray, Graham J. / Expression of cannabinoid CB1 receptors by vagal afferent neurons: Kinetics and role in influencing neurochemical phenotype. In: AJP: Gastrointestinal and Liver Physiology. 2010 ; Vol. 299, No. 1. pp. G63-G69.

Bibtex

@article{4acc52afcb5c490b9df504b7cd80f620,
title = "Expression of cannabinoid CB1 receptors by vagal afferent neurons: Kinetics and role in influencing neurochemical phenotype",
abstract = "The intestinal hormone cholecystokinin (CCK) inhibits food intake via stimulation of vagal afferent neurons (VAN). Recent studies suggest that CCK also regulates the expression of some G protein-coupled receptors and neuropeptide transmitters in these neurons. The aim of the present study was to characterize the expression of cannabinoid (CB)1 receptors in VAN and to determine whether stimulation of these receptors plays a role in regulating neurochemical phenotype. Expression of CB1 in rat VAN was detectable by in situ hybridization or immunohistochemistry after 6 h of fasting and increased to a maximum after 24 h when ∼50{\%} of neurons in the mid and caudal regions expressed the receptor. Melanin-concentrating hormone (MCH)1 receptors also increased with fasting, but the changes were delayed compared with CB1; in contrast Y2 receptors (Y2R) exhibited reciprocal changes in expression to CB1. Administration of CCK8s (10 nmol ip) to fasted rats decreased expression of CB1 with a t1/2 of ∼1 h compared with 3 h for MCH1. The action of CCK8s was inhibited by ghrelin and orexin-A. The CB1 agonist anandamide (intraperitoneally) reversed the effect of CCK8s on CB1, MCH1, and Y2 receptor expression. In contrast, in rats fasted for 18 h, administration of a CB1 antagonist/inverse agonist (AM281 ip) downregulated CB1 expression and increased Y2 receptor expression. Activation of vagal CB1 receptors therefore influences the neurochemical phenotype of these neurons, indicating a new and hitherto unrecognized role for endocannabinoids in gut-brain signaling. Copyright {\circledC} 2010 the American Physiological Society.",
keywords = "Cholecystokinin, Endocannabinoid, Melanin-concentrating hormone-1 receptor, Nodose ganglion, Y2 receptor",
author = "Galina Burdyga and Andrea Varro and Rod Dimaline and Thompson, {David G.} and Dockray, {Graham J.}",
year = "2010",
month = "7",
doi = "10.1152/ajpgi.00059.2010",
language = "English",
volume = "299",
pages = "G63--G69",
journal = "American Journal of Physiology: Gastrointestinal and Liver Physiology",
issn = "0193-1857",
publisher = "American Physiological Society",
number = "1",

}

RIS

TY - JOUR

T1 - Expression of cannabinoid CB1 receptors by vagal afferent neurons: Kinetics and role in influencing neurochemical phenotype

AU - Burdyga, Galina

AU - Varro, Andrea

AU - Dimaline, Rod

AU - Thompson, David G.

AU - Dockray, Graham J.

PY - 2010/7

Y1 - 2010/7

N2 - The intestinal hormone cholecystokinin (CCK) inhibits food intake via stimulation of vagal afferent neurons (VAN). Recent studies suggest that CCK also regulates the expression of some G protein-coupled receptors and neuropeptide transmitters in these neurons. The aim of the present study was to characterize the expression of cannabinoid (CB)1 receptors in VAN and to determine whether stimulation of these receptors plays a role in regulating neurochemical phenotype. Expression of CB1 in rat VAN was detectable by in situ hybridization or immunohistochemistry after 6 h of fasting and increased to a maximum after 24 h when ∼50% of neurons in the mid and caudal regions expressed the receptor. Melanin-concentrating hormone (MCH)1 receptors also increased with fasting, but the changes were delayed compared with CB1; in contrast Y2 receptors (Y2R) exhibited reciprocal changes in expression to CB1. Administration of CCK8s (10 nmol ip) to fasted rats decreased expression of CB1 with a t1/2 of ∼1 h compared with 3 h for MCH1. The action of CCK8s was inhibited by ghrelin and orexin-A. The CB1 agonist anandamide (intraperitoneally) reversed the effect of CCK8s on CB1, MCH1, and Y2 receptor expression. In contrast, in rats fasted for 18 h, administration of a CB1 antagonist/inverse agonist (AM281 ip) downregulated CB1 expression and increased Y2 receptor expression. Activation of vagal CB1 receptors therefore influences the neurochemical phenotype of these neurons, indicating a new and hitherto unrecognized role for endocannabinoids in gut-brain signaling. Copyright © 2010 the American Physiological Society.

AB - The intestinal hormone cholecystokinin (CCK) inhibits food intake via stimulation of vagal afferent neurons (VAN). Recent studies suggest that CCK also regulates the expression of some G protein-coupled receptors and neuropeptide transmitters in these neurons. The aim of the present study was to characterize the expression of cannabinoid (CB)1 receptors in VAN and to determine whether stimulation of these receptors plays a role in regulating neurochemical phenotype. Expression of CB1 in rat VAN was detectable by in situ hybridization or immunohistochemistry after 6 h of fasting and increased to a maximum after 24 h when ∼50% of neurons in the mid and caudal regions expressed the receptor. Melanin-concentrating hormone (MCH)1 receptors also increased with fasting, but the changes were delayed compared with CB1; in contrast Y2 receptors (Y2R) exhibited reciprocal changes in expression to CB1. Administration of CCK8s (10 nmol ip) to fasted rats decreased expression of CB1 with a t1/2 of ∼1 h compared with 3 h for MCH1. The action of CCK8s was inhibited by ghrelin and orexin-A. The CB1 agonist anandamide (intraperitoneally) reversed the effect of CCK8s on CB1, MCH1, and Y2 receptor expression. In contrast, in rats fasted for 18 h, administration of a CB1 antagonist/inverse agonist (AM281 ip) downregulated CB1 expression and increased Y2 receptor expression. Activation of vagal CB1 receptors therefore influences the neurochemical phenotype of these neurons, indicating a new and hitherto unrecognized role for endocannabinoids in gut-brain signaling. Copyright © 2010 the American Physiological Society.

KW - Cholecystokinin

KW - Endocannabinoid

KW - Melanin-concentrating hormone-1 receptor

KW - Nodose ganglion

KW - Y2 receptor

U2 - 10.1152/ajpgi.00059.2010

DO - 10.1152/ajpgi.00059.2010

M3 - Article

VL - 299

SP - G63-G69

JO - American Journal of Physiology: Gastrointestinal and Liver Physiology

JF - American Journal of Physiology: Gastrointestinal and Liver Physiology

SN - 0193-1857

IS - 1

ER -