Hippocampal GLP-1 Receptors Influence Food Intake, Meal Size, and Effort-Based Responding for Food through Volume Transmission
Open accessAbstract
Glucagon-like peptide-1 (GLP-1) is produced in the small intestines and in nucleus tractus solitarius (NTS) neurons. Activation of central GLP-1 receptors (GLP-1Rs) reduces feeding and body weight. The neural circuits mediating these effects are only partially understood. Here we investigate the inhibition of food intake and motivated responding for food in rats following GLP-1R activation in the ventral hippocampal formation (HPFv), a region only recently highlighted in food intake control. Increased HPFv GLP-1R activity following exendin-4 administration potently reduced food intake (both chow and Western diet) and body weight, whereas HPFv GLP-1R blockade increased food intake. These hypophagic effects were based on reduced meal size, and likely do not involve nausea as HPFv exendin-4 did not induce a conditioned flavor avoidance. HPFv GLP-1R activation also reduced effort-based responding for food under an operant progressive ratio reinforcement schedule, but did not affect food conditioned place preference expression. To investigate possible routes of HPFv GLP-1 signaling, immunohistochemical analysis revealed the absence of GLP-1 axon terminals in the HPFv, suggesting volume transmission as a mechanism of action. Consistent with this, the presence of active GLP-1 was detected in both the cerebrospinal fluid (CSF) and the HPFv. The source of CSF GLP-1 may be NTS GLP-1-producing neurons, as, (1) ∼30% of NTS GLP-1 neurons colocalized with the retrograde tracer fluorogold (FG) following lateral ventricle FG injection, and (2) GLP-1-immunoreactive axon terminals were observed adjacent to the ventricular ependymal layer. Collectively these findings illuminate novel neuronal and behavioral mechanisms mediating food intake reduction by GLP-1.
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A subset of GLP-1R neuron populations behind the blood-brain barrier likely represents common targets, which are both accessible to peripherally administered GLP-1RAs (probably only upon chronic dosing) and to endogenous GLP-1 released from PPGs via synapses and/or cerebrospinal fluid-mediated volume transmission.
“Finally, a subset of GLP-1R neuron populations behind the blood-brain barrier likely represents common targets, which are both accessible to peripherally administered GLP-1RAs (probably only upon chronic dosing) and to endogenous GLP-1 released from PPGs via synapses and/or cerebrospinal fluid–mediated volume transmission (15, 16, 69).”
From GLP-1 and the Neurobiology of Eating Control: Recent Advances (2025) · cites this paper as [69]
The individual necessity of distinct GLP-1R neuron populations for the anorectic and weight loss effects of GLP-1RAs has now been claimed by multiple studies using various loss-of-function approaches in rodents.
“The individual necessity of distinct GLP-1R neuron populations for the anorectic and weight loss effects of GLP-1RAs has now been claimed by multiple studies using various loss-of-function approaches in rodents (47, 50‐54, 69).”
From GLP-1 and the Neurobiology of Eating Control: Recent Advances (2025) · cites this paper as [69]
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- Authors
- Hsu, T. M., Hahn, J. D., Konanur, V. R., Lam, A., & Kanoski, S. E.
- Affiliations
- University of Southern California (US)
- Corresponding author
- Kanoski, Scott E
- Venue
- Neuropsychopharmacology
- Published
- 2014-07-18
- Volume
- 40
- Issue
- 2
- Pages
- 327-337
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC4443945
- OpenAlex
- W2029549266
- Cited by
- 176
- References
- 59
- Citations by year
- 2026: 12 · 2025: 29 · 2024: 15 · 2023: 13 · 2022: 17 · 2021: 19 · 2020: 16 · 2019: 10 · 2018: 12 · 2017: 9 · 2016: 11 · 2015: 11 · 2014: 2
- FWCI
- 5.35
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eli Lilly and Company
- National Institute of Diabetes and Digestive and Kidney Diseases (DK097147, DK102478, K01DK097147, R03DK102478)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- GLP-1 receptor, dietary intake, meal size, volume transmission, exendin-4, nucleus tractus solitarius, weight loss, Western diet, retrograde tracing
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Exenatide, Animals, Animal Feed, Avoidance Learning, Axons, Conditioning, Psychological, Eating, Feeding Behavior, Hippocampus, Hypoglycemic Agents, Male, Motivation, Neurons, Peptides, Reinforcement Schedule, Rhombencephalon, Spatial Behavior, Venoms, Rats, Sprague-Dawley, Taste Perception
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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