1. It has been hypothesized that psychotic symptoms in depression may be du
e to increased dopamine activity secondary to hypothalamic-pituitary-adrena
l (HPA) axis overactivity.
2. To test this hypothesis, the authors examined the cortisol response to d
examethasone suppression test (DST, 1mg orally) and multihormonal responses
to apomorphine (APO, 0.75 mg S.C.)-a dopamine agonist-in 150 drug-free hos
pitalized patients with DSM-IV major depressive episode with psychotic feat
ures (MDEP, n=35), major depressive episode without psychotic features (MDE
, n=74), or schizophrenia paranoid type (SCZ, n=41), and 27 hospitalized he
althy controls (HCs).
3. MDEPs showed increased activity of the HPA system (i.e. higher post-DST
cortisol levels) than HCs, SCZs and MDEs. However, there were no difference
s in adrenocorticotropic hormone (ACTH), cortisol, prolactin and growth hor
mone (GH) responses to APO between MDEPs and MDEs and HCs. On the other han
d, SCZs showed lower APO-induced ACTH stimulation and a higher rate of blun
ted GH than HCs, MDEs and MDEPs, suggesting a functional alteration of the
hypothalamic dopamine receptors in SCZs.
4. In the total sample and in each diagnostic group, DST suppressors and no
n-suppressors showed no differences in hormonal responses to APO.
5: These results suggest a lack of causal link between HPA axis hyperactivi
ty and dopamine dysregulation. In contrast to schizophrenia, psychotic symp
toms in depression seem not to be related to dopamine function dysregulatio
n.