ArticlePsychopharmacology2012
Restricted role of CRF1 receptor for the activity of brainstem catecholaminergic neurons in the negative state of morphine withdrawal.
Article in Psychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Propranolol Administration During Morphine Addiction Attenuates Reinstatement of Drug-Aversive Memories Caused by Exposure to Stressful Stimuli.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Effects of CB1 receptor negative allosteric modulator Org27569 on oxycodone withdrawal symptoms in mice.Psychopharmacology · 2024Article
- Drug addiction co-morbidity with alcohol: Neurobiological insights.International review of neurobiology · 2021Review
- Corticotropin-Releasing Factor (CRF) and Addictive Behaviors.International review of neurobiology · 2017Review
- Alterations of naltrexone-induced conditioned place avoidance by pre-exposure to high fructose corn syrup or heroin in Sprague-Dawley rats.Psychopharmacology · 2016Article
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- Corticotropin releasing factor: a key role in the neurobiology of addiction.Frontiers in neuroendocrinology · 2014Review
- Corticotropin-releasing factor (CRF) receptor-1 is involved in cardiac noradrenergic activity observed during naloxone-precipitated morphine withdrawal.British journal of pharmacology · 2014Article
- Effect of berberine on depression- and anxiety-like behaviors and activation of the noradrenergic system induced by development of morphine dependence in rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2012Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleEvidence suggests that corticotropin-releasing factor (CRF) system is an important mediator in the negative symptoms of opioid withdrawal.
objectivesWe used genetically engineered mice lacking functional CRF receptor-1 (CRF1R) levels to study the role for CRF/CRF1R pathways in the negative affective states of opioid withdrawal.
methodsWild-type and CRF1R(-/-) offspring of CRF1R(+/-) breeders were identified by PCR analysis of tail DNA and were rendered dependent on morphine via intraperitoneal injection of increasing doses of morphine (10-60 mg/kg). Negative state associated with opioid withdrawal was examined by using conditioned place aversion (CPA), TH expression and TH phosphorylation were measured in different brain regions involved in addictive behaviours using immunohistochemistry.
resultsThe weight loss in morphine withdrawn CRF1R(-/-) animals was significantly (p < 0.05) lower versus wild-type. The aversion for environmental cues paired with opioid withdrawal was lower (p < 0.001) in the CRF1R-deficient versus wild-type. Using dual immunolabeling for c-Fos, data show that naloxone-induced withdrawal increases the number of TH positive neurons phosphorylated at Ser40 or Ser31 that coexpress c-Fos in the nucleus of tractus solitarius (NTS)-A2 from wild-type and CRF(-/-) deficient mice. By contrast, the number of phospho-Ser40 or phospho-Ser31 positive neurons expressing c-Fos was lower in the ventrolateral medulla (VLM)-A1 in CRF(-/-)-deficient mice.
conclusionOur study demonstrates an increased activity of brainstem catecholaminergic neurons after CPA induced by morphine withdrawal suggesting that CRF1R is implicated in the activation of A1 neurons and provides evidence that this receptor is involved in the body weight loss and in the negative aversive effects of morphine withdrawal.
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