Glucocorticoids and mammalian motor nerve excitability.
Short-term treatment of cats with high doses of triamcinolone and related steroids strikingly increased the capacity of soleus motoneurons to generate posttetanic stimulus-bound repetition (SBR) and the obligatory postetanic potentiation (PTP) of muscle. The edrophonium chloride (Tensillon)-induced SBR and twitch potentiation were likewise augmented. These effects reflect an increase in the excitability of the motoneuron. This glucocorticoid effect suggests that the motoneuron is the site of the antimyasthenic action of the hormone. Certainly, the enhanced SBR is a neuronal representation of the adverse epileptogenic action of the glucocorticoids. The glucocorticoid effect on motoneuron outlasts the dosing period, suggesting an underlying alteration in the neuron. Other glucocorticoids caused the same effects, but varied in their potencies. Mineralocorticoids were less effective. The single androgen that was tested proved to be minimally effective.
D000818:Animals; D002415:Cats; D002712:Chlorides / Q000097:blood; D003900:Desoxycorticosterone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005071:Evoked Potentials / Q000187:drug effects*; D005260:Female; D005438:Fludrocortisone / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology*; D008297:Male; D009046:Motor Neurons / Q000187:drug effects*; D009119:Muscle Contraction / Q000187:drug effects; D009277:Nandrolone / Q000494:pharmacology; D011188:Potassium / Q000097:blood; D011239:Prednisolone / Q000494:pharmacology; D012964:Sodium / Q000097:blood; D014221:Triamcinolone / Q000008:administration & dosage / Q000494:pharmacology
D002712:Chlorides; D005938:Glucocorticoids; D014221:Triamcinolone; D003900:Desoxycorticosterone; D009277:Nandrolone; D012964:Sodium; D011239:Prednisolone; D011188:Potassium; D005438:Fludrocortisone