Abstract
Systemic administration of ACTH to rats with normal hormone production induced a rapid (started 3 min postinjection) and long-term (persisted 30 min) elevation of pain threshold. Complete inhibition of glucocorticoid production shortened the duration of ACTH-induced analgesia to 15 min. The biphasic effect of ACTH on pain sensitivity is probably mediated by short-term glucocorticoid-independent and long-term glucocorticoid-dependent mechanisms.
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