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Am J Physiol Regul Integr Comp Physiol. 2015 Jan 1;308(1):R1-9. doi: 10.1152/ajpregu.00388.2014. Epub 2014 Nov 12.

NMDA-type glutamate receptors participate in reduction of food intake following hindbrain melanocortin receptor activation.

Author information

1
Department of Integrative Physiology and Neuroscience, College of Veterinary Medicine, Washington State University, Pullman, Washington.
2
Department of Integrative Physiology and Neuroscience, College of Veterinary Medicine, Washington State University, Pullman, Washington britter@vetmed.wsu.edu.

Abstract

Hindbrain injection of a melanocortin-3/4 receptor agonist, MTII, reduces food intake primarily by reducing meal size. Our previously reported results indicate that N-methyl-D-aspartate-type glutamate receptors (NMDAR) in the nucleus of the solitary tract (NTS) play an important role in the control of meal size and food intake. Therefore, we hypothesized that activation of NTS NMDARs contribute to reduction of food intake in response to fourth ventricle or NTS injection of MTII. We found that coinjection of a competitive NMDAR antagonist (d-CPP-ene) with MTII into the fourth ventricle or directly into the NTS of adult male rats attenuated MTII-induced reduction of food intake. Hindbrain NMDAR antagonism also attenuated MTII-induced ERK1/2 phosphorylation in NTS neurons and prevented synapsin I phosphorylation in central vagal afferent endings, both of which are cellular mechanisms previously shown to participate in hindbrain melanocortinergic reduction of food intake. Together, our results indicate that NMDAR activation significantly contributes to reduction of food intake following hindbrain melanocortin receptor activation, and it participates in melanocortinergic signaling in NTS neural circuits that mediate reduction of food intake.

KEYWORDS:

nucleus of the solitary tract; proopiomelanocortin; satiation; vagus

PMID:
25394828
PMCID:
PMC4281681
DOI:
10.1152/ajpregu.00388.2014
[Indexed for MEDLINE]
Free PMC Article

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