Detection of G Protein-coupled Receptor Expression in Mouse Vagal Afferent Neurons using Multiplex In Situ Hybridization

10.3791/62945 ◽  
2021 ◽  
Author(s):  
Johnson Bob-Manuel ◽  
Laurent Gautron
Keyword(s):  
G Protein ◽  
Receptor Expression ◽  
Afferent Neurons ◽  
G Protein Coupled Receptor ◽  
Vagal Afferent ◽  
G Protein Coupled

scholarly journals Expression of cannabinoid CB1 receptors by vagal afferent neurons: kinetics and role in influencing neurochemical phenotype

2010 ◽  
Vol 299 (1) ◽  
pp. G63-G69 ◽  
Author(s):  
Galina Burdyga ◽  
Andrea Varro ◽  
Rod Dimaline ◽  
David G. Thompson ◽  
Graham J. Dockray
Keyword(s):  
Receptor Expression ◽  
Cb1 Receptors ◽  
Afferent Neurons ◽  
Y2 Receptor ◽  
Melanin Concentrating Hormone ◽  
Cb1 Antagonist ◽  
Vagal Afferent ◽  
G Protein Coupled ◽  
Stimulation Of

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.

scholarly journals Anatomical Profiling of G Protein-Coupled Receptor Expression

Cell ◽  
2008 ◽  
Vol 135 (3) ◽  
pp. 561-571 ◽  
Author(s):  
Jean B. Regard ◽  
Isaac T. Sato ◽  
Shaun R. Coughlin
Keyword(s):  
G Protein ◽  
Receptor Expression ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled

G protein-coupled receptor expression in Halobacterium salinarum

2001 ◽  
pp. 141-159 ◽  
Author(s):  
Ann M. Winter-Vann ◽  
Lynell Martinez ◽  
Cynthia Bartus ◽  
Agata Levay ◽  
George J. Turner
Keyword(s):  
G Protein ◽  
Halobacterium Salinarum ◽  
Receptor Expression ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled

scholarly journals Repetitive Activation of Hypothalamic G Protein-Coupled Receptor 54 with Intravenous Pulses of Kisspeptin in the Juvenile Monkey (Macaca mulatta) Elicits a Sustained Train of Gonadotropin-Releasing Hormone Discharges

Endocrinology ◽  
2006 ◽  
Vol 147 (2) ◽  
pp. 1007-1013 ◽  
Author(s):  
Tony M. Plant ◽  
Suresh Ramaswamy ◽  
Meloni J. DiPietro
Keyword(s):  
G Protein ◽  
Concomitant Treatment ◽  
Secondary Effects ◽  
G Protein Coupled Receptor ◽  
Gnrh Release ◽  
Dependent Signal ◽  
Lh Release ◽  
Lh Secretion ◽  
G Protein Coupled

The purpose of the present study was to further examine the hypothesis that activation of G protein-coupled receptor 54 (GPR54) signaling at the end of the juvenile phase of primate development is responsible for initiation of gonadarche and the onset of puberty. Accordingly, we determined whether repetitive iv administration of the GPR54 receptor agonist kisspeptin-10 (2 μg as a brief 1-min infusion once every hour for 48 h) to the juvenile male rhesus monkey would prematurely elicit sustained, pulsatile release of hypothalamic GnRH, the neuroendocrine trigger for gonadarche. GnRH release was monitored indirectly by measuring LH secretion from the in situ pituitary, the GnRH responsiveness of which had been heightened before the experiment with an intermittent iv infusion of synthetic GnRH. Agonadal animals (n = 4) were employed to eliminate any confounding and secondary effects of changing feedback signals from the testis. The first brief infusion of kisspeptin-10 evoked an LH discharge that mimicked those produced by GnRH priming, and this was followed by a train of similar LH discharges in response to hourly activation of GPR54 by repetitive kisspeptin-10 administration. Concomitant treatment with a GnRH receptor antagonist, acyline, abolished kisspeptin-10-induced LH release. Repetitive kisspeptin-10 administration also provided a GnRH-dependent signal to FSH secretion. These findings are consistent with the notion that, in primates, the transition from the juvenile (attenuated GnRH release) to pubertal (robust GnRH release) state is controlled by activation of GPR54 resulting from increased expression of hypothalamic KiSS-1 and release of kisspeptin in this region of the brain.

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