Reward devaluation and heroin escalation is associated with differential expression of CRF signaling genes
Autor: | Kent E. Vrana, Caesar G. Imperio, Ashley J. McFalls, Willard M. Freeman, Georgina V. Bixler, Patricia S. Grigson |
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Rok vydání: | 2016 |
Předmět: |
Male
0301 basic medicine Corticotropin-Releasing Hormone media_common.quotation_subject Prefrontal Cortex Hippocampus Self Administration Nucleus accumbens Nucleus Accumbens 03 medical and health sciences chemistry.chemical_compound Saccharin 0302 clinical medicine Reward Gene expression medicine Animals Prefrontal cortex media_common Heroin Dependence General Neuroscience Addiction Ventral Tegmental Area Rats Heroin Ventral tegmental area 030104 developmental biology medicine.anatomical_structure chemistry Cues Signal transduction Psychology Neuroscience hormones hormone substitutes and hormone antagonists 030217 neurology & neurosurgery |
Zdroj: | Brain Research Bulletin. 123:81-93 |
ISSN: | 0361-9230 |
Popis: | One of the most damaging aspects of drug addiction is the degree to which natural rewards (family, friends, employment) are devalued in favor of seeking, obtaining and taking drugs. We have utilized an animal model of reward devaluation and heroin self-administration to explore the role of the coricotropin releasing factor (CRF) pathway. Given access to a saccharin cue followed by the opportunity to self-administer heroin, animals will parse into distinct phenotypes that suppress their saccharin intake (in favor of escalating heroin self-administration) or vice versa. We find that large saccharin suppressors (large heroin takers) demonstrate increased mRNA expression for elements of the CRF signaling pathway (CRF, CRF receptors and CRF binding protein) within the hippocampus, medial prefrontal cortex and the ventral tegmental area. Moreover, there were no gene expression changes of these components in the nucleus accumbens. Use of bisulfite conversion sequencing suggests that changes in CRF binding protein and CRF receptor gene expression may be mediated by differential promoter methylation. |
Databáze: | OpenAIRE |
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