Role for hypocretin in mediating stress-induced reinstatement of cocaine-seeking behavior.
paper
Cited
Public
Unavailable
- Authors
- Boutrel, Benjamin; Kenny, Paul J; Specio, Sheila E; Martin-Fardon, RΓ©mi; Markou, Athina; Koob, George F; de Lecea, Luis
- Year
- 2005
- Journal
- Proceedings of the National Academy of Sciences of the United States of America
- PMID
- 16357203
- DOI
- 10.1073/pnas.0507480102
- PMCID
- PMC1323172
Hypocretin-1 and -2 (Hcrt-1 and Hcrt-2), also referred to as orexin-A and -B, are neuropeptides synthesized by a few thousand neurons in the lateral hypothalamus. Hypocretin-containing neurons project throughout the brain, with a prominent input to basal forebrain structures involved in motivation, reward, and stress. However, the role of hypocretins in addiction-related behaviors remains largely unexplored. Here we show that intracerebroventricular infusions of Hcrt-1 lead to a dose-related reinstatement of cocaine seeking without altering cocaine intake in rats. Hcrt-1 also dramatically elevates intracranial self-stimulation thresholds, indicating that, unlike treatments with reinforcing properties such as cocaine, Hcrt-1 negatively regulates the activity of brain reward circuitries. Hypocretin-induced reinstatement of cocaine seeking was prevented by blockade of noradrenergic and corticotropin-releasing factor systems, suggesting that Hcrt-1 reinstated drug seeking through induction of a stress-like state. Consistent with this interpretation, the selective Hcrt-1 receptor antagonist SB-334867 blocked footshock-induced reinstatement of previously extinguished cocaine-seeking behavior. These findings reveal a previously unidentified role for hypocretins in driving drug seeking through activation of stress pathways in the brain.
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