PubMed · 7704728
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A D Rogol. 1994. Hypopituitarism.. https://pubmed.ncbi.nlm.nih.gov/7704728/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Explore the source record for details and available documents.
BACKGROUND: The aim of this work was to investigate alterations of plasma corticotropin-releasing factor (CRF) levels in depressive states. We have also measured plasma cortisol and corticotropin (ACTH) concentrations and examined their correlation with the peripheral CRF values. METHODS: Thirty-six outpatients from the psychiatric department of a Barcelona hospital who were diagnosed as having major depressive disorder (n = 26) and dysthymic depressive disorder (n = 10) were studied. Among the major depressed patients, 10 suffered from severe depressive disorder and 16 from mild or moderate depressive disorder. The comparison group consisted of 17 healthy volunteers. Cortisol, ACTH, and CRF concentrations were determined by iodine-125 radioimmunoassay; CRF measurements were performed on C18 extracted samples. RESULTS: CRF and cortisol plasma concentrations were significantly higher in major depression and dysthymia than in the comparison group. The major depressed patients did not show significantly different CRF and cortisol levels than the dysthymic. Severe major depressive disorder exhibited significantly higher CRF plasma levels than the mild or moderate episodes. Plasma cortisol and CRF concentrations correlated significantly. CONCLUSIONS: The results obtained indicate that plasma CRF values are altered in depressive disorders and suggest that these determinations could be important for understanding the pathophysiology in affective illness.
Stress may contribute to the increased vulnerability to and the development of cocaine addiction. Corticotropin-releasing factor (CRF) activates the hypothalamic-pituitary-adrenal (HPA) axis as well as behavioral and immune processes in response to different environmental and pharmacologic stressors. We hypothesized that CRF might mediate some of the effects of cocaine and as such it may be a link between stressful events and increased vulnerability to cocaine addiction. We demonstrated that blockade of endogenous CRF by a CRF antiserum or a receptor antagonist prevented the cocaine-induced corticosterone response in rats. In male rhesus monkeys and in humans, cocaine selectively increased the amplitude-related, CRF-dependent, elements of pulsatile ACTH release. Cocaine-induced locomotor hyperactivity was antagonized by intracerebroventricular (i.c.v.) administration of a CRF antiserum and a CRF receptor antagonist in rats. In rhesus monkeys, strong correlations were found between behavioral hyperactivity and CRF-dependent elements of pulsatile activity of the HPA axis. Acute cocaine administration induced dose- and time-dependent alterations in hypothalamic and extrahypothalamic/limbic CRF concentrations in rats. Cocaine withdrawal elicited anxiety-like behavior and alterations of CRF concentration in the hypothalamus, amygdala, and basal forebrain. CRF antiserum (i.c.v.) antagonized anxiety-like behavior related to cocaine withdrawal. These data strongly suggest that the HPA axis, brain CRF in particular, may mediate some of the neuroendocrine and behavioral effects of cocaine. The potential involvement of CRF and HPA axis in cocaine-induced psychopathology is hypothesized.