ArticleNeuropharmacology2018
GLP-1 action in the mouse bed nucleus of the stria terminalis.
Article in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Can GLP-1 Be a Target for Reward System Related Disorders? A Qualitative Synthesis and Systematic Review Analysis of Studies on Palatable Food, Drugs of Abuse, and Alcohol.Frontiers in behavioral neuroscience · 2020Pooled it
- Alcohol abstinence precipitates alcohol seeking and aversion-resistant intake in association with increased BNST activity.Molecular psychiatry · 2026Article
- The central amygdala gates exogenous glucagon-like peptide 1 signals.Molecular metabolism · 2026Article
- A Distinct Subpopulation of Extended Amygdala Neurons Drives Food Intake.Biological psychiatry global open science · 2026Article
- Diet-induced obesity impairs refeeding responses and downregulates lateral septal GLP-1R in male rats: an effect reversed by weight-loss treatment.Frontiers in pharmacology · 2026Article
- The estrous cycle moderates the food and body weight suppressive effects of glucagon-like peptide-1 receptor agonism.Diabetes, obesity & metabolism · 2026Article
- Crosstalk between alcohol use disorder and obesity: two sides of the same coin?Molecular psychiatry · 2025Review
- Brain-Derived GLP-1-Understanding the Physiological Function and Anti-obesity Potential of Preproglucagon Neurons.Endocrinology · 2025Review
- Integration of Glucagon-Like Peptide 1 Receptor Actions Through the Central Amygdala.Endocrinology · 2025Review
- Novel neural pathways targeted by GLP-1R agonists and bariatric surgery.Pflugers Archiv : European journal of physiology · 2025Review
- Role of the bed nucleus of the stria terminalis in feeding.Frontiers in nutrition · 2025Review
- Hunting for heroes: Brain neurons mediating GLP-1R agonists in obesity treatment.Obesity medicine · 2024Article
- BNST GluN2D-containing NMDARs contribute to ethanol intake but not negative affective behaviors in female mice.Alcohol, clinical & experimental research · 2024Article
- The gut-brain axis in appetite, satiety, food intake, and eating behavior: Insights from animal models and human studies.Pharmacology research & perspectives · 2024Review
- Positive Effects of Adiponectin, BDNF, and GLP-1 on Cortical Neurons Counteracting Palmitic Acid Induced Neurotoxicity.Clinical nutrition research · 2024Article
- Glucagon-like peptide-1 facilitates cerebellar parallel fiber glutamate release through PKA signaling in mice in vitro.Scientific reports · 2023Article
- RISING STARS: Targeting G protein-coupled receptors to regulate energy homeostasis.Journal of molecular endocrinology · 2023Review
- GLP-1 enhances hyperpolarization-activated currents of mouse cerebellar Purkinje cellFrontiers in molecular neuroscience · 2023Article
- Antismoking agents do not contribute synergistically to semaglutide's ability to reduce alcohol intake in rats.Frontiers in pharmacology · 2023Article
- Activation of arcuate nucleus glucagon-like peptide-1 receptor-expressing neurons suppresses food intake.Cell & bioscience · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Glucagon-like peptide-1 (GLP-1) injected into the brain reduces food intake. Similarly, activation of preproglucagon (PPG) cells in the hindbrain which synthesize GLP-1, reduces food intake. However, it is far from clear whether this happens because of satiety, nausea, reduced reward, or even stress. Here we explore the role of the bed nucleus of the stria terminalis (BNST), an area involved in feeding control as well as stress responses, in GLP-1 responses. Using cre-expressing mice we visualized projections of NTS PPG neurons and GLP-1R-expressing BNST cells with AAV-driven Channelrhodopsin-YFP expression. The BNST displayed many varicose YFP+ PPG axons in the ventral and less in the dorsal regions. Mice which express RFP in GLP-1R neurons had RFP+ cells throughout the BNST with the highest density in the dorsal part, suggesting that PPG neuron-derived GLP-1 acts in the BNST. Indeed, injection of GLP-1 into the BNST reduced chow intake during the dark phase, whereas injection of the GLP-1 receptor antagonist Ex9 increased feeding. BNST-specific GLP-1-induced food suppression was less effective in mice on high fat (HF, 60%) diet, and Ex9 had no effect. Restraint stress-induced hypophagia was attenuated by BNST Ex9 treatment, further supporting a role for endogenous brain GLP-1. Finally, whole-cell patch clamp recordings of RFP+ BNST neurons demonstrated that GLP-1 elicited either a depolarizing or hyperpolarizing reversible response that was of opposite polarity to that under dopamine. Our data support a physiological role for BNST GLP-1R in feeding, and suggest complex cellular responses to GLP-1 in this nucleus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.