243. Dopaminergic function and HPA axis activity in psychotic depression

It has been hypothesized that psychotic symptoms in depression may be due to increased dopamine activity secondary to hypothalamic-pituitary-adrenal (HPA) axis overactivity. To test this hypothesis we examined the cortisol response to dexamethasone suppression test (DST, 1 mg orally) and multihormonal responses to apomorphine (APO, 0.75 mg SC)—a dopamine agonist—in 123 drug-free DSM-IV severely-depressed inpatients: 81 without psychotic features (SD; 35M/46F; mean age ± SD, 38.1 ± 10.6 years) and 42 with psychotic features (SDP; 19M/23F; mean age 39.1 ± 9.7 years); and 36 hospitalized controls (HC; 15M/21F; mean age 35.8 ± 9.1 years). SDPs showed increased activity of the HPA system (i.e. higher post-DST cortisol levels) than HCs (p < 0.00001) and SDs (p < 0.00002). Although APO-induced cortisol stimulation was lower in SDPs than in HCs (p < 0.04)—owing to a baseline cortisol effect—there were no differences in adrenocorticotropic hormone (ACTH), prolactin (PRL), and growth hormone (GH) responses to APO between SDPs and SDs and HCs. Moreover, in the total sample and in each diagnostic group, DST suppressors and DST non-suppressors showed no differences in hormonal responses to APO. Therefore, our study indicates that dopaminergic function, as assessed by the APO test, does not differ between psychotic and nonpsychotic depressed patients, although HPA disinhibition occurs more frequently in psychotic depressed patients. These results suggest that there is no causal link between HPA axis hyperactivity and dopamine dysfunction at the hypothalamic-pituitary level in psychotic depressed patients.