ArticleNeuropharmacology2015
Knockdown of steroid receptors in the central nucleus of the amygdala induces heightened pain behaviors in the rat.
Article in Neuropharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed, 40 citations in OpenAlex.
- Amygdala electrical stimulation for operant conditioning in rat navigation.Biomedical engineering letters · 2024Article
- Environmental enrichment reverses stress-induced changes in the brain-gut axis to ameliorate chronic visceral and somatic hypersensitivity.Neurobiology of stress · 2024Article
- Stress-induced visceral pain in female rats is associated with epigenetic remodeling in the central nucleus of the amygdala.Neurobiology of stress · 2021Article
- Environmental enrichment prevents stress-induced epigenetic changes in the expression of glucocorticoid receptor and corticotrophin releasing hormone in the central nucleus of the amygdala to inhibit visceral hypersensitivity.Experimental neurology · 2021Article
- Central amygdala mineralocorticoid receptors modulate alcohol self-administration.Neuropharmacology · 2020Article
- Environmental enrichment prevents chronic stress-induced brain-gut axis dysfunction through a GR-mediated mechanism in the central nucleus of the amygdala.Neurogastroenterology and motility · 2020Article
- Sex differences in the epigenetic regulation of chronic visceral pain following unpredictable early life stress.Neurogastroenterology and motility · 2020Article
- Inhibition of Microglial Activation in the Amygdala Reverses Stress-Induced Abdominal Pain in the Male Rat.Cellular and molecular gastroenterology and hepatology · 2020Article
- Colitis-Induced Microbial Perturbation Promotes Postinflammatory Visceral Hypersensitivity.Cellular and molecular gastroenterology and hepatology · 2020Article
- Animal Models for Functional Gastrointestinal Disorders.Frontiers in psychiatry · 2020Review
- Role of estrogen and stress on the brain-gut axis.American journal of physiology. Gastrointestinal and liver physiology · 2019Review
- Targeting epigenetic mechanisms for chronic visceral pain: A valid approach for the development of novel therapeutics.Neurogastroenterology and motility · 2019Review
- Mechanisms of Stress-induced Visceral Pain.Journal of neurogastroenterology and motility · 2018Review
- Stereotaxic Exposure of the Central Nucleus of the Amygdala to Corticosterone Increases Colonic Permeability and Reduces Nerve-Mediated Active Ion Transport in Rats.Frontiers in neuroscience · 2018Article
- Orexins Mediate Sex Differences in the Stress Response and in Cognitive Flexibility.Biological psychiatry · 2017Article
- Stress-Induced Chronic Visceral Pain of Gastrointestinal Origin.Frontiers in systems neuroscience · 2017Review
- 2015 James W. Freston Single Topic Conference: A Renaissance in the Understanding and Management of Irritable Bowel Syndrome.Cellular and molecular gastroenterology and hepatology · 2016Article
- The effect of sex and irritable bowel syndrome on HPA axis response and peripheral glucocorticoid receptor expression.Psychoneuroendocrinology · 2016Article
- 2015 James W. Freston Single Topic Conference: A Renaissance in the Understanding and Management of Irritable Bowel Syndrome.Gastroenterology · 2016Article
- Sex-related differences in pain behaviors following three early life stress paradigms.Biology of sex differences · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Previously we demonstrated that exposure of the central nucleus of the amygdala (CeA) to elevated corticosterone (CORT) induces nociceptive behaviors that are reversed by glucocorticoid and/or mineralocorticoid (GR/MR) receptor antagonism. Here we test the hypothesis that in a cholesterol (CHOL)-implanted control rat, selective knockdown of GR/MR in the CeA would, via a corticotropin-releasing factor (CRF)-mediated mechanism, replicate the nociceptive behaviors produced by elevated amygdala CORT. Micropellets of CHOL or CORT were stereotaxically placed on the dorsal margin of the CeA. Cannulae were implanted into the CeA for the delivery of vehicle or oligodeoxynucleotide (ODN) of either antisense (ASO) or random sequences (RSO) targeting GR or MR. Visceromotor behavioral response quantified visceral sensitivity in response to colonic distension, while von Frey filaments assessed somatic sensitivity. Receptor expression was determined with qRT-PCR. In CHOL implanted controls, knockdown of GR in the CeA increased both colonic and somatic sensitivity, whereas selective knockdown of MR in the CeA induced colonic hypersensitivity without affecting somatic sensitivity. CRF expression in the CeA was increased in CHOL-implanted rats treated with GR or MR ASO and resembled the augmented CRF expression seen in the CORT-implanted rats. This is the first study to demonstrate that decreasing either GR or MR within the CeA is sufficient to induce visceral hypersensitivity whereas somatic hypersensitivity developed after only GR knockdown. The loss of either GR or MR was associated with an increased CRF expression, and may represent a common mechanism for the development of CeA-mediated nociceptive behaviors.
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What OpenQuestion holds
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.