Alterations in corticotropin-releasing factor and vasopressin content in rat brain during morphine withdrawal: correlation with hypothalamic noradrenergic activity and pituitary-adrenal response.

The modification in the activity of noradrenergic neurons projecting to the hypothalamus and the pituitary-adrenal response during morphine withdrawal as well its correlation with alterations in corticotropin-releasing factor (CRF) and vasopressin (AVP) content in different brain areas was analyzed. Male rats were implanted with placebo (naïve) or morphine (tolerant/dependent) pellets for 7 days. On day 8, groups of rats received an acute injection of saline s.c. (control) or naloxone (1 mg/kg s.c.) and were decapitated 30 min later. After administration of naloxone to tolerant rats (withdrawal) we found a striking parallelism between an enhanced activity of hypothalamic noradrenergic neurons and an increased corticosterone secretion; concomitantly, the CRF but not the AVP content in the paraventricular nucleus was decreased, which might reflect an increased release of the peptide. During withdrawal, CRF content also was decreased in the arcuate nucleus, whereas no changes were found in the median eminence, dorsomedial, ventromedial nuclei or in the bed nucleus of the stria terminalis. AVP content levels were not modified in arcuate nucleus, supraoptic or in the suprachiasmatic nuclei. Present data suggest that a hypothalamic noradrenergic hypersecretion may be involved in a selectively increased activity of CRF neurons in the paraventricular nucleus and arcuate nucleus and then in the enhanced release of corticosterone induced by morphine withdrawal. However, we did not find any correlation between opioid withdrawal-induced alterations in the pituitary-adrenal axis and AVP modifications.

• Publication year

  1998

• Venue

  Journal of Pharmacology and Experimental Therapeutics

• Publication date

  1998-05-01

• Fields of study

  Medicine, Chemistry

• Identifiers
  DOI 10.1016/s0022-3565(24)37420-8PMID 9580616
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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