A reappraisal of the effects of ACTH on the response of the central nervous system to injury.
ACTH possesses powerful immuno-suppressive properties and also retards healing by inhibiting fibroblast proliferation and the deposition of collagen. In the present work this hormone was used to test both the 'barrier' and 'immune' hypotheses relating to the failure of CNS regeneration after injury, dosages being administered which had been found to stimulate maximal adrenal production of glucocorticoids in control animals. Although the scarring in the CNS and the systemic humoral and cellular immune responses were significantly depressed, no increase in CNS axon growth was noted, even when large doses of thyroxine were added. We conclude that both 'immune' and 'barrier' hypotheses should be rejected, and that the beneficial effects of thyroxine treatment reported by some workers are not substantiated.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D000917:Antibody Formation / Q000187:drug effects; D001921:Brain / Q000473:pathology; D001930:Brain Injuries / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*; D002452:Cell Count; D007111:Immunity, Cellular / Q000187:drug effects; D007165:Immunosuppression Therapy; D051379:Mice; D009416:Nerve Regeneration / Q000187:drug effects*; D051381:Rats; D014945:Wound Healing / Q000187:drug effects
D000324:Adrenocorticotropic Hormone