Effect of naloxone-precipitated morphine withdrawal on c- fos expression in rat corticotropin-releasing hormone neurons in the paraventricular hypothalamus and extended amygdala

• Published in: Neuroscience letters Vol. 362; no. 1; pp. 39 - 43
• Main Authors: Hamlin, A.S., Buller, K.M., Day, T.A., Osborne, P.B.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 13.05.2004; Elsevier
• Subjects: Amygdala; Amygdala - drug effects; Amygdala - metabolism; Animals; Biological and medical sciences; c-fos; Corticotropin-releasing hormone; Corticotropin-Releasing Hormone - biosynthesis; Corticotropin-Releasing Hormone - genetics; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation - drug effects; Gene Expression Regulation - physiology; Immunohistochemistry; Male; Morphine - pharmacology; Morphine withdrawal; Naloxone - pharmacology; Neurons - drug effects; Neurons - metabolism; Paraventricular Hypothalamic Nucleus - drug effects; Paraventricular Hypothalamic Nucleus - metabolism; Paraventricular hypothalamus; Proto-Oncogene Proteins c-fos - biosynthesis; Proto-Oncogene Proteins c-fos - genetics; Rats; Rats, Wistar; Substance Withdrawal Syndrome - genetics; Substance Withdrawal Syndrome - metabolism; Vertebrates: nervous system and sense organs; Immunohistochemistry; c-fos; Morphine withdrawal; Amygdala; Corticotropin-releasing hormone; Paraventricular hypothalamus; Rat; Rodentia; Central nervous system; Corticotropin releasing factor; Morphine; Basal ganglion; Hypothalamus; Gene expression; Encephalon; Hypothalamic hormone; Vertebrata; Mammalia; Naloxone; Neuron; Animal; Hormone releasing factor; Protooncogene; Immediate early gene
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2004.02.033

Morphine withdrawal is characterized by physical symptoms and a negative affective state. The 41 amino acid polypeptide corticotropin-releasing hormone (CRH) is hypothesized to mediate, in part, both the negative affective state and the physical withdrawal syndrome. Here, by means of dual-immunohistochemical methodology, we examined the co-expression of the c-Fos protein and CRH following naloxone-precipitated morphine withdrawal. Rats were treated with slow-release morphine 50 mg/kg (subcutaneous, s.c.) or vehicle every 48 h for 5 days, then withdrawn with naloxone 5 mg/kg (s.c.) or saline 48 h after the final morphine injection. Two hours after withdrawal rats were perfused transcardially and their brains were removed and processed for immunohistochemistry. We found that naloxone-precipitated withdrawal of morphine-dependent rats increased c-Fos immunoreactivity (IR) in CRH positive neurons in the paraventricular hypothalamus. Withdrawal of morphine-dependent rats also increased c-Fos-IR in the central amygdala and bed nucleus of the stria terminalis, however these were in CRH negative neurons.