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Adult male rats with chronic indwelling intracerebroventricular (i.c.v.) and jugular catheters were given an i.c.v. injection (over 1 min) of 1, 10, 100 ng or 1 µg ACTH(1–24), or 300 ng ACTH(4–10) or saline, and blood samples were taken 0, 5, 15, 30 and 60 min later. Increasing dosages of ACTH(1–24) caused a dose-related rise in serum LH levels. Peak levels of serum LH (ranging from 157 to 473% of pretreatment levels) were reached 5–15 min after treatment, and then serum LH values returned to pretreatment levels by 60 min. The serum LH response to 1 µg ACTH(1–24) did not differ from the response to 100 ng ACTH(1–24). Administration (i.c.v.) of 300 ng ACTH(4–10) was also effective in increasing serum LH values. Repeated withdrawal of blood during the experiment increased serum corticosterone values in all groups including saline-treated), but i.c.v. administration of ACTH(1–24) or ACTH(4–10) did not further increase serum corticosterone levels. Two additional groups of rats were injected i.p. with either saline or pentobarbital (30 mg/kg body weight) 1 h before i.c.v. administration of 10 ng ACTH(1–24) and blood samples were taken as in the other groups. The animals in these groups did not show a rise in serum LH concentrations in response to ACTH(1–24). In a third experiment, rats were pretreated (i.c.v.) with either ACTH antiserum (ACTH-Ab) or normal rabbit serum 15 min before a 2-min ether stress. The ether stress evoked a significant rise in serum LH concentrations within 15 min. Serum LH levels then fell below the 0-min value by 60 min. Pretreatment with ACTH-Ab failed to alter the serum LH response to this acute stress. The failure of ACTH-Ab to alter the response to stress suggests that the central nervous system ACTH does not play a physiological role in this process. Alternatively, we cannot be certain that the potency of the ACTH-Ab was sufficient to neutralize central nervous system ACTH effectively.

J. Endocr. (1986) 108, 275–280