Ga. Charles et al., ARECOLINE REVERSES DEXAMETHASONE SUPPRESSION OF CORTISOL IN NORMAL MALES - A PILOT-STUDY, Biological psychiatry, 37(11), 1995, pp. 811-816
Six normal controls participated in two or three individual, intraveno
us challenges (each separated by 1 week) of saline or one of two doses
of arecoline at 8 AM following ingestion of 1 mg dexamethasone at 12
midnight the previous evening. Individuals differed in their subjectiv
e and neuroendocrine responses to arecoline. At 2.1 mu g/kg (n = 4) or
2.8 mu g/kg (n = 1), four of five subjects evidenced dexamethone supp
ression test (DST) nonsuppression, which followed the rise in prolacti
n. Cholinergic side effects and nausea were minimal. At a dose of 4.2
mu g/kg, four of five subjects evidenced cortisol escape from dexameth
asone suppression, which was associated with a substantial vise in pro
lactin, some subjective cholinergic symptoms, and little to modest nau
sea, These data are consistent with the notion that cholinergic mechan
isms are involved in the escape from dexamethasone suppression. Furthe
r, arecoline may be preferable to physostigmine as a cholinergic agoni
st, since it appears less likely to cause marked cholinergic side effe
cts and significant nausea.