Medial prefrontal cortex neuropeptide Y modulates binge-like ethanol consumption in C57BL/6J mice
| العنوان: | Medial prefrontal cortex neuropeptide Y modulates binge-like ethanol consumption in C57BL/6J mice |
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| المؤلفون: | Isabel M Marrero, Carlos A. Perez-Heydrich, Todd E. Thiele, Kathryn J. Reissner, Marian T. Sepulveda-Orengo, Stacey L. Robinson |
| المصدر: | Neuropsychopharmacology |
| بيانات النشر: | Springer Science and Business Media LLC, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | Male, medicine.medical_specialty, Efferent, Population, Prefrontal Cortex, behavioral disciplines and activities, Article, Binge Drinking, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Limbic system, Internal medicine, Neural Pathways, medicine, Animals, Neuropeptide Y, Prefrontal cortex, Receptor, education, Pharmacology, education.field_of_study, Ethanol, Basolateral Nuclear Complex, Chemistry, musculoskeletal, neural, and ocular physiology, Neuropeptide Y receptor, Receptors, Neuropeptide Y, 030227 psychiatry, Mice, Inbred C57BL, Disease Models, Animal, Psychiatry and Mental health, medicine.anatomical_structure, Endocrinology, nervous system, Female, psychological phenomena and processes, 030217 neurology & neurosurgery, Basolateral amygdala |
| الوصف: | Neuropeptide Y (NPY) signaling via limbic NPY1 and 2 receptors (NPY1R and NPY2R, respectively) is known to modulate binge-like ethanol consumption in rodents. However, the role of NPY signaling in the medial prefrontal cortex (mPFC), which provides top-down modulation of the limbic system, is unknown. Here, we used "drinking-in-the-dark" (DID) procedures in C57BL/6J mice to address this gap in the literature. First, the impact of DID on NPY immunoreactivity (IR) was assessed in the mPFC. Next, the role of NPY1R and NPY2R signaling in the mPFC on ethanol consumption was evaluated through site-directed pharmacology. Chemogenetic inhibition of NPY1R+ neurons in the mPFC was performed to further evaluate the role of this population. To determine the potential role of NPY1R+ neurons projecting from the mPFC to the basolateral amygdala (BLA) this efferent population was selectively silenced. Three, 4-day cycles of DID reduced NPY IR in the mPFC. Intra-mPFC activation of NPY1R and antagonism of NPY2R resulted in decreased binge-like ethanol intake. Silencing of mPFC NPY1R+ neurons overall, and specifically NPY1R+ neurons projecting to the BLA, significantly reduced binge-like ethanol intake. We provide novel evidence that (1) binge-like ethanol intake reduces NPY levels in the mPFC; (2) activation of NPY1R or blockade of NPY2R reduces binge-like ethanol intake; and (3) chemogenetic inhibition of NPY1R+ neurons in the mPFC and NPY1R+ mPFC neurons projecting to the BLA blunts binge-like drinking. These observations provide the first direct evidence that NPY signaling in the mPFC modulates binge-like ethanol consumption. |
| تدمد: | 1740-634X 0893-133X |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::da3c5e136fec3080ee1ea69affd8570cTest https://doi.org/10.1038/s41386-018-0310-7Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....da3c5e136fec3080ee1ea69affd8570c |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 1740634X 0893133X |
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