Corticotropin-Releasing Factor Within the Central Nucleus of the Amygdala and the Nucleus Accumbens Shell Mediates the Negative Affective State of Nicotine Withdrawal in Rats
Autor: | S. Alex Marshall, Daria Rylkova, Melissa Prado, Catherine A. Marcinkiewcz, Adrie W. Bruijnzeel, Shani Isaac |
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Rok vydání: | 2009 |
Předmět: |
Male
Nicotine medicine.medical_specialty Corticotropin-Releasing Hormone media_common.quotation_subject Self Administration Nicotinic Antagonists Mecamylamine Nucleus accumbens reward deficit Amygdala Nucleus Accumbens Article 03 medical and health sciences 0302 clinical medicine Internal medicine medicine Animals Nicotinic Agonists Rats Wistar 030304 developmental biology media_common Pharmacology 0303 health sciences Dose-Response Relationship Drug Mood Disorders Central nucleus of the amygdala Addiction corticotropin-releasing factor dependence medicine.disease Rats Substance Withdrawal Syndrome Disease Models Animal Psychiatry and Mental health Stria terminalis Endocrinology Nicotine withdrawal medicine.anatomical_structure Brain stimulation reward Psychology psychological phenomena and processes 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology |
ISSN: | 1740-634X 0893-133X |
Popis: | Tobacco addiction is a chronic disorder that is characterized by a negative affective state upon smoking cessation and relapse after periods of abstinence. Previous research has shown that an increased central release of corticotropin-releasing factor (CRF) at least partly mediates the deficit in brain reward function associated with nicotine withdrawal in rats. The aim of these studies was to investigate the role of CRF in the central nucleus of the amygdala (CeA), the lateral bed nucleus of the stria terminalis (BNST), and the nucleus accumbens shell (Nacc shell) in the deficit in brain reward function associated with precipitated nicotine withdrawal. The intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Elevations in brain reward thresholds are indicative of a deficit in brain reward function. In all experiments, the nicotinic receptor antagonist mecamylamine (3 mg/kg) elevated the brain reward thresholds of the nicotine-dependent rats (9 mg/kg per day of nicotine salt) and did not affect the brain reward thresholds of the saline-treated control rats. The administration of the nonspecific CRF1/2 receptor antagonist D-Phe CRF((12-41)) into the CeA and the Nacc shell prevented the mecamylamine-induced elevations in brain reward thresholds in the nicotine-dependent rats. Blockade of CRF1/2 receptors in the lateral BNST did not prevent the mecamylamine-induced elevations in brain reward thresholds in the nicotine-dependent rats. These studies indicate that the negative emotional state associated with precipitated nicotine withdrawal is at least partly mediated by an increased release of CRF in the CeA and the Nacc shell. |
Databáze: | OpenAIRE |
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