Orexin-A Hyperphagia: Hindbrain Participation in Consummatory Feeding Responses
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Orexin-A (ORXA) is an orexigenic neuropeptide produced by the lateral hypothalamus that increases food intake when injected into the brain ventricles or forebrain nuclei. We used a licking microstructure analysis to evaluate hindbrain and forebrain ORXA effects in intact and hindbrain-lesioned rats, to identify the motivational and anatomical bases of ORXA hyperphagia. Intact rats with cannulas in the fourth brain ventricle (4V) received vehicle (artificial cerebrospinal fluid) or ORXA (0.1, 0.4, 1, or 10 nm) injections before 90 min access to 0.1 m sucrose. Meal size and frequency were increased in a double-dissociated manner by the 1 and 10 nm doses, respectively. In experiment 2, 4V 1 nm ORXA was applied to rats offered solutions varied in caloric and gustatory intensity (water and 0.1 and 1 m sucrose). ORXA increased meal frequency for all tastants. ORXA increased meal size only for 0.1 m sucrose, by prolonging the meal without affecting early ingestion rate or lick burst size, suggesting that 4V ORXA influenced inhibitory postingestive feedback rather than taste evaluation. In experiment 3, rats with cannulas in the third ventricle (3V) received dorsal medullary lesions centered on the area postrema (APX group) or sham procedures, and licking for water and 0.1 and 1 m sucrose was evaluated after 1 nm 3V ORXA/artificial cerebrospinal fluid injections. The 3V ORXA increased 0.1 m sucrose meal size and meal frequency for all tastants in the sham group, as observed after 4V ORXA in experiment 2. In the APX group, 3V ORXA injections influenced meal frequency, but they no longer increased meal size. However, the APX rats increased meal size for 0.1 m sucrose after food and water deprivation and after 3V angiotensin II injection. They also showed meal size suppression after 3V injection of the melanocortin-3/4 receptor agonist melanotan II (1 nm). These findings suggest that the area postrema and subjacent nucleus of the solitary tract are necessary for increases in consummatory (meal size) but not appetitive (meal frequency) responses to 3V ORXA. The meal size increases may be due to reduced postingestive feedback inhibition induced by ORXA delivered to either the hindbrain or forebrain ventricles. Orexin-A increases meal size via gut feedback disinhibition, not enhanced gustatory evaluation. Medullary lesions abolish meal size but not frequency increases, indicating dissociable sites for orexin-A feeding actions.
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Orexin neurons project widely within both forebrain and hindbrain, including a hypothalamic-thalamic-striatal loop and projections to oromotor and autonomic motor areas in the caudal brainstem.
“In addition to midbrain dopamine neurons, orexin neurons project widely within both forebrain and hindbrain. In particular, a hypothalamic-thalamic-striatal loop involving orexin projections to the paraventricular nucleus of the thalamus and cholinergic striatal interneurons ([93](#B93)), and orexin projections to oromotor and autonomic motor areas in the caudal brainstem ([6](#B6)).”
From Food reward, hyperphagia, and obesity (2011) · cites this paper as [6]
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- Authors
- Baird, J.-P., Choe, A., Loveland, J. L., Beck, J., Mahoney, C. E., Lord, J. S., & Grigg, L. A.
- Affiliations
- Amherst College (US)
- Corresponding author
- Baird, John-Paul
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2008-11-13
- Volume
- 150
- Issue
- 3
- Pages
- 1202-1216
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC2654731
- OpenAlex
- W2143492384
- Cited by
- 65
- References
- 81
- Citations by year
- 2024: 3 · 2023: 2 · 2022: 3 · 2021: 3 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 3 · 2015: 10 · 2014: 7 · 2013: 7 · 2012: 6
- FWCI
- 1.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Digital Library (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- Amherst College
- National Institutes of Health
- National Institute on Deafness and Other Communication Disorders (DC07389, R15DC007389)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- orexin-A, hyperphagia, meal size, meal frequency, area postrema, nucleus tractus solitarius, dorsal medulla, lateral hypothalamus, licking behavior, melanocortin 3/4 receptor, melanotan II, angiotensin II, food and water deprivation, sucrose
- MeSH terms
- Orexins, Animals, Appetite, Behavior, Animal, Dose-Response Relationship, Drug, Eating, Feeding Behavior, Hyperphagia, Infusion Pumps, Injections, Intraventricular, Male, Neuropeptides, Rhombencephalon, Taste, Rats, Sprague-Dawley, Intracellular Signaling Peptides and Proteins, Rats
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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