ArticleMolecular metabolism2015
The role of GluN2A and GluN2B NMDA receptor subunits in AgRP and POMC neurons on body weight and glucose homeostasis.
Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 40 citations in OpenAlex.
- How muscle talks to brain: apelin protein mediates exercise-induced antidepressant effects.Molecular psychiatry · 2026Article
- From brain bioenergetics to hypothalamic glucoregulation: A shared-systems hypothesis for intrinsic dysglycemia in schizophrenia.Reviews in endocrine & metabolic disorders · 2026Review
- An obligatory role for AgRP neurons in maintaining body temperature during time-restricted feeding.Metabolism: clinical and experimental · 2026Article
- Neuronal surface P antigen (NSPA) as a novel regulator of energy homeostasis and adipose tissue metabolism.Molecular medicine (Cambridge, Mass.) · 2026Article
- An obligatory role for AgRP neurons in maintaining body temperature during time-restricted feeding.bioRxiv : the preprint server for biology · 2025Article
- Tryptophan Metabolism in Obesity: The Indoleamine 2,3-Dioxygenase-1 Activity and Therapeutic Options.Advances in experimental medicine and biology · 2024Review
- CPT1A in AgRP neurons is required for sex-dependent regulation of feeding and thirst.Biology of sex differences · 2023Article
- EphrinB1 modulates glutamatergic inputs into POMC-expressing progenitors and controls glucose homeostasis.PLoS biology · 2020Article
- Transcriptomic analysis links diverse hypothalamic cell types to fibroblast growth factor 1-induced sustained diabetes remission.Nature communications · 2020Article
- Postnatal Overnutrition Induces Changes in Synaptic Transmission to Leptin Receptor-Expressing Neurons in the Arcuate Nucleus of Female Mice.Nutrients · 2020Article
- Role of POMC and AgRP neuronal activities on glycaemia in mice.Scientific reports · 2019Article
- Remote control of glucose-sensing neurons to analyze glucose metabolism.American journal of physiology. Endocrinology and metabolism · 2018Review
- p53 in AgRP neurons is required for protection against diet-induced obesity via JNK1.Nature communications · 2018Article
- A High-fat, High-sugar 'Western' Diet Alters Dorsal Striatal Glutamate, Opioid, and Dopamine Transmission in Mice.Neuroscience · 2018Article
- Regulation of Hippocampal Synaptic Function by the Metabolic Hormone, Leptin: Implications for Health and Neurodegenerative Disease.Frontiers in cellular neuroscience · 2018Review
- Effect of developmental NMDAR antagonism with CGP 39551 on aspartame-induced hypothalamic and adrenal gene expression.PloS one · 2018Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveHypothalamic agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) expressing neurons play critical roles in control of energy balance. Glutamatergic input via n-methyl-d-aspartate receptors (NMDARs) is pivotal for regulation of neuronal activity and is required in AgRP neurons for normal body weight homeostasis. NMDARs typically consist of the obligatory GluN1 subunit and different GluN2 subunits, the latter exerting crucial differential effects on channel activity and neuronal function. Currently, the role of specific GluN2 subunits in AgRP and POMC neurons on whole body energy and glucose balance is unknown.
methodsWe used the cre-lox system to genetically delete GluN2A or GluN2B only from AgRP or POMC neurons in mice. Mice were then subjected to metabolic analyses and assessment of AgRP and POMC neuronal function through morphological studies.
resultsWe show that loss of GluN2B from AgRP neurons reduces body weight, fat mass, and food intake, whereas GluN2B in POMC neurons is not required for normal energy balance control. GluN2A subunits in either AgRP or POMC neurons are not required for regulation of body weight. Deletion of GluN2B reduces the number of AgRP neurons and decreases their dendritic length. In addition, loss of GluN2B in AgRP neurons of the morbidly obese and severely diabetic leptin-deficient Lep (ob/ob) mice does not affect body weight and food intake but, remarkably, leads to full correction of hyperglycemia. Lep (ob/ob) mice lacking GluN2B in AgRP neurons are also more sensitive to leptin's anti-obesity actions.
conclusionsGluN2B-containing NMDA receptors in AgRP neurons play a critical role in central control of body weight homeostasis and blood glucose balance via mechanisms that likely involve regulation of AgRP neuronal survival and structure, and modulation of hypothalamic leptin action.
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