Evidence map›Paper›PMID 24957819›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014

Amylin receptor signaling in the nucleus accumbens negatively modulates μ-opioid-driven feeding.

Sarah K Baisley, Brian A Baldo

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. The long-acting amylin/calcitonin receptor agonist ZP5461 suppresses food intake and body weight in male rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. An amylin analogue attenuates alcohol-related behaviours in various animal models of alcohol use disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    Article
  13. Article
  14. Review
  15. Article
  16. Physiologic and Neural Controls of Eating.Gastroenterology clinics of North America · 2016
    Review
  17. Review
  18. Endogenous VMH amylin signaling is required for full leptin signaling and protection from diet-induced obesity.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  19. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Sarah K BaisleyNeuroscience Training Program, University of Wisconsin-Madison, Medical Sciences Center, University Ave Madison, WI, USA.
Brian A Baldo1] Neuroscience Training Program, University of Wisconsin-Madison, Medical Sciences Center, University Ave Madison, WI, USA [2] Department of Psychiatry University of Wisconsin-Madison, Research Park Blvd, Madison, WI, USA.
University of Wisconsin–Madison · US

Funding

NEUROSCIENCE TRAINING PROGRAMT32GM007507 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI HALLORAN, MARY C · 1985 to 2017
$9.3M
AMY-1 receptors: Novel targets for antipsychotic developmentR21MH093824 · NIMH · UNIVERSITY OF WISCONSIN-MADISON · PI BAKSHI, VAISHALI P, BALDO, BRIAN A · 2011 to 2012
$408k
NIGMS NIH HHS T32 GM007507NIMH NIH HHS R21 MH093824
6 · The paper itself

Abstract

Amylin is a peptide co-secreted with insulin that penetrates into the brain, and produces satiation-like effects via actions in the brainstem, hypothalamus, and mesencephalon. Little is known, however, about the effects of amylin in the nucleus accumbens shell (AcbSh), where a circumscribed zone of intense amylin receptor (AMY-R) binding overlaps reported mappings of a 'hotspot' for μ-opioid receptor (μ-OR) amplification of food reward. Here, the ability of intra-AcbSh AMY-R signaling to modulate μ-OR-driven feeding was explored. Amylin (1-30 ng) was administered with the μ-OR agonist, D-Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO) (0.25 μg), directly into the AcbSh of ad libitum-maintained rats. Amylin dose-dependently reversed DAMGO-induced hyperphagia; 3 ng of amylin reduced DAMGO-mediated feeding by nearly 50%. This dose was, however, completely ineffective at altering DAMGO-induced feeding in the anterior dorsal striatum. Intra-AcbSh amylin alone (3-30 ng) modestly suppressed 10% sucrose intake in ad libitum-maintained rats, and chow in food-deprived rats, but only at the 30-ng dose. This result indicates that reversal of AcbSh DAMGO-induced feeding at a 10-fold lower dose was neither due to malaise nor motoric impairment. Finally, intra-AcbSh infusion of the AMY-R antagonist, AC187 (20 μg), significantly attenuated the ability of prefeeding to suppress DAMGO-induced food intake, with no effects in non-prefed rats. Hence, AMY-R signaling negatively modulates μ-OR-mediated appetitive responses at the level of the AcbSh. The results with AC187 indicate that endogenous AMY-R transmission in the AcbSh curtails opioid function in the postprandial period, suggesting a novel pathway for peripheral-central integration in the control of appetitive motivation and opioid reward.

Indexed as

Analgesics, OpioidAnalysis of VarianceAnimalsDose-Response Relationship, DrugEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Feeding BehaviorFood PreferencesIslet Amyloid PolypeptideMaleNucleus AccumbensPeptide FragmentsRatsRats, Sprague-DawleyReceptors, Islet Amyloid PolypeptideReceptors, Opioid, muSignal TransductionAC 187Analgesics, OpioidEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Islet Amyloid PolypeptidePeptide FragmentsReceptors, Islet Amyloid PolypeptideReceptors, Opioid, mu

Identifiers

PMID24957819
PMCPMC4229571
OpenAlexW2058981227

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.