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Titolo:
DISSOCIATION BETWEEN BEHAVIORAL AND HORMONAL RESPONSES TO THE FORCED SWIM STRESS IN LACTATING RATS
Autore:
WALKER CD; TROTTIER G; ROCHFORD J; LAVALLEE D;
Indirizzi:
MCGILL UNIV,DOUGLAS HOSP,RES CTR,DEPT PSYCHIAT,6875 LASALLE BLVD MONTREAL PQ H4H 1R3 CANADA
Titolo Testata:
Journal of neuroendocrinology
fascicolo: 8, volume: 7, anno: 1995,
pagine: 615 - 622
SICI:
0953-8194(1995)7:8<615:DBBAHR>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALARM SUBSTANCE; ANTIDEPRESSANT ACTIVITY; PITUITARY; CORTICOSTERONE; ADRENALECTOMY; REVERSAL; )D-ALA2,MET5>ENKEPHALINAMIDE; GLUCOCORTICOIDS; DEPRESSION; RETENTION;
Keywords:
LACTATION; ACTH; CORTICOSTERONE; FORCED SWIM TEST;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
C.D. Walker et al., "DISSOCIATION BETWEEN BEHAVIORAL AND HORMONAL RESPONSES TO THE FORCED SWIM STRESS IN LACTATING RATS", Journal of neuroendocrinology, 7(8), 1995, pp. 615-622

Abstract

Retention of immobility in the Porsolt forced swim test is believed to be dependent upon glucocorticoid secretion in male rats. Because lactating females exhibit increased basal glucocorticoid secretion and blunted stress responses, we tested the hypothesis that lactation-induced changes in adrenal glucocorticoid and in circulating estrogen and progesterone levels would improve retention and/or acquisition of immobility. Immobility was recorded during 3 intervals of 5 min on day 1 (acquisition) and one 5 min interval 24 h later (retention). Blood samples were collected before the swim test and at various times after the onset of stress for plasma ACTH and corticosterone (B) determinations. Male rats (young = 200 g, old = 325 g) were compared to virgin females(V) and to lactating females in early (day 8-10, EL) and late (day 17-19, LL) lactation. Adrenalectomy (ADX) and ovariectomy (OVX) were performed 5 and 10 days prior to testing, respectively. All animals acquired immobility at the end of the 15 min swim on day 1, but only the young male group exhibited a significant retention of immobility on day 2. Total immobility was higher in males than females (V) although basal and stress-induced ACTH and B secretion were comparable on both testing days. Lactational status did not affect immobility in either the acquisition or retention phases. However, stress-induced ACTH secretionwas greatly diminished in intact and ADX lactating females (EL and LL) compared to virgins (LL < EL < virgin), demonstrating a clear dissociation between behavioral and neuroendocrine responses, Following ADX,immobility in the retention phase was either decreased in males or increased in lactating females. Finally, OVX decreased immobility in both lactating (EL) and virgin females without significantly altering themagnitude of the ACTH and B responses to stress. In summary, our results demonstrated both sex-related and lactation-related differences inthe behavioral and endocrine responses to the forced swim test of Porsolt. Although retention of the immobile response is thought to involve glucocorticoids and/or opioids secreted during the first testing session, we did not find evidence for a direct relationship between basalor stress-induced total corticosterone secretion, the magnitude of ACTH response to stress and behavioral scores in the retention period. However, experimental variables such as body weight, sex and water depth could significantly modify the outcome of behavioral testing and question the validity of glucocorticoid-mediated retention processes. Since the effect of ADX was reversed in lactating females compared to male rats, we hypothesize that glucocorticoid sensitivity of cognitive processes controlling behavioral reactivity is different from that controlling hypothalamic-adrenocortical function. Our results also demonstrated a clear dissociation between behavioral and neuroendocrine responses to the swim test, in particular during lactation. In early and late lactation, blunted responsiveness to stress was not caused by enhanced glucocorticoid feedback but might result from modifications in the inhibitory and/or stimulatory inputs to hypothalamic neurons controlling adrenocortical activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 04:52:36