The effect of acute administration of the opioid receptor antagonist naloxone hydrochloride (5 mg/kg, s.c.) on plasma LH levels was evaluated in female and male rats 24, 36 and 48 h and 1, 3 and 5 weeks after gonadectomy and in 5-week gonadectomized rats after acute or acronic (2 weeks) administration of oestradiol benzoate (OB, 10 μg/rat per day, s.c.), testosterone propionate (TP, 150 μg/rat, s.c.) or dihydrotestosterone propionate (DHT, 150 μg/rat, s.c.) respectively. Concurrent evaluation of plasma LH after administration of LH releasing hormone (LHRH, 1 μg/kg i.p.) was performed in the same experimental groups. In rats of both sexes, a significant rise in plasma LH after naloxone was observed in sham-operated and recently gonadectomized rats (24-48 h); in female rats 36 and 48 h after gonadectomy the rise was higher than in controls. One, 3 and 5 weeks after gonadectomy, naloxone failed to stimulate LH release in both female and male rats. In gonadectomized rats undergoing steroid replacement therapy, OB administered 72 h before testing, TP (16 and 72 h) and DHT (16 h) were the most effective in reinstituting the LH response to naloxone. Chronic administration of gonadal steroids did not restore normal LH responsiveness to naloxone. In most experimental groups, LH responses after naloxone were clearly unrelated to pituitary LH responsiveness to LHRH, which indicates that the opioid antagonist was acting via the central nervous system. In conclusion, these results demonstrate that: (1) gonadal steroids are critically important for the inhibitory effect of endogenous opioids on LH secretion to be manifested; (2) inhibition by the opiatergic system on LH secretion is more dependent on a modulatory action of gonadal steroids than on their simple presence or absence.

Petraglia, F., Locatelli, V., Penalva, A., Cocchi, D., Genazzani, A.R., & Müller, E.E. (1984). Gonadal steroid modulation of naloxone-induced LH secretion in the rat. JOURNAL OF ENDOCRINOLOGY, 101(1), 33-39 [10.1677/joe.0.1010033].

Gonadal steroid modulation of naloxone-induced LH secretion in the rat

Petraglia, F.;
1984

Abstract

The effect of acute administration of the opioid receptor antagonist naloxone hydrochloride (5 mg/kg, s.c.) on plasma LH levels was evaluated in female and male rats 24, 36 and 48 h and 1, 3 and 5 weeks after gonadectomy and in 5-week gonadectomized rats after acute or acronic (2 weeks) administration of oestradiol benzoate (OB, 10 μg/rat per day, s.c.), testosterone propionate (TP, 150 μg/rat, s.c.) or dihydrotestosterone propionate (DHT, 150 μg/rat, s.c.) respectively. Concurrent evaluation of plasma LH after administration of LH releasing hormone (LHRH, 1 μg/kg i.p.) was performed in the same experimental groups. In rats of both sexes, a significant rise in plasma LH after naloxone was observed in sham-operated and recently gonadectomized rats (24-48 h); in female rats 36 and 48 h after gonadectomy the rise was higher than in controls. One, 3 and 5 weeks after gonadectomy, naloxone failed to stimulate LH release in both female and male rats. In gonadectomized rats undergoing steroid replacement therapy, OB administered 72 h before testing, TP (16 and 72 h) and DHT (16 h) were the most effective in reinstituting the LH response to naloxone. Chronic administration of gonadal steroids did not restore normal LH responsiveness to naloxone. In most experimental groups, LH responses after naloxone were clearly unrelated to pituitary LH responsiveness to LHRH, which indicates that the opioid antagonist was acting via the central nervous system. In conclusion, these results demonstrate that: (1) gonadal steroids are critically important for the inhibitory effect of endogenous opioids on LH secretion to be manifested; (2) inhibition by the opiatergic system on LH secretion is more dependent on a modulatory action of gonadal steroids than on their simple presence or absence.
Petraglia, F., Locatelli, V., Penalva, A., Cocchi, D., Genazzani, A.R., & Müller, E.E. (1984). Gonadal steroid modulation of naloxone-induced LH secretion in the rat. JOURNAL OF ENDOCRINOLOGY, 101(1), 33-39 [10.1677/joe.0.1010033].
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11365/33175
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