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Expression data from adult mouse hypothalamus

ABSTRACT: Chronic dietary aspartame may impair rodent insulin tolerance and may affect behavior. Previous studies have shown the aspartame effects may be modulated by developmental NMDA receptor antagonism. Present study was designed to assess effects of aspartame and NMDAR antagonism on components of the HPA axis. We used microarray analysis to examine changes in adult rodent hypothalamic gene expression following chronic aspartame exposure and/or developmental NMDA receptor antagonism.

ORGANISM(S): Mus musculus

PROVIDER: GSE100325 | GEO | 2018/03/11

REPOSITORIES: GEO

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Expression data from adult mouse adrenal tissue

Project description:Chronic dietary aspartame may impair rodent insulin tolerance and may affect behavior. Previous studies have shown the aspartame effects may be modulated by developmental NMDA receptor antagonism. Present study was designed to assess effects of aspartame and NMDAR antagonism on components of the HPA axis. We used microarray analysis to examine changes in adult rodent adrenal gene expression following chronic aspartame exposure and/or developmental NMDA receptor antagonism.

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Effects of developmental N-Methyl D-aspartate (NMDA) receptor antagonism on adulthood hypothalamic gene expression in female C57Bl/6J mice.

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Effects of developmental N-Methyl D-aspartate (NMDA) receptor antagonism on adulthood adrenal gene expression in female C57Bl/6J mice.

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Effect of developmental NMDAR antagonism on aspartame-induced hypothalamic and adrenal gene expression

Project description:Effect of developmental NMDAR antagonism on aspartame-induced hypothalamic and adrenal gene expression

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GLP-1 directed NMDA receptor antagonism for obesity treatment [I]

Project description:The N-methyl-d-aspartate (NMDA) receptor is a glutamate-activated cation channel critical to many processes in the brain. Genome-wide association studies (GWAS) suggest that glutamatergic neurotransmission and NMDA receptor-mediated synaptic plasticity is important for body weight homeostasis1. Here, we report the engineering and preclinical development of a first-in-class bimodal molecule that integrates NMDA receptor antagonism with glucagon-like peptide-1 (GLP-1) receptor agonism to effectively reverse obesity, hyperglycemia, and dyslipidemia in rodent models of metabolic disease. We demonstrate that GLP-1-directed delivery of the NMDA receptor antagonist MK-801 affects NMDA receptor-mediated synaptic plasticity in the hypothalamus. Importantly, peptide-targeting of MK-801 specifically to GLP-1 receptor-expressing brain regions circumvent adverse physiological and behavioral effects associated with MK-801 monotherapy. In sum, our approach demonstrates the feasibility of cell specific ionotropic receptor-modulation via peptide targeting and highlights the therapeutic potential of unimolecular mixed GLP-1 receptor agonism and NMDA receptor antagonism for obesity treatment.

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