CHOLINERGIC AND ADRENERGIC-FUNCTION IN DEPRESSED AND HEALTHY-SUBJECTS- A NEUROENDOCRINE TEST BATTERY USING THE GROWTH-HORMONE AXIS

The two neurotransmitters noradrenaline (NA) and acetylcholine (ACh), both important modulators of GH secretion, have been hypothesised to b e reciprocally dysfunctional in depressive illness. This study tested the Adrenergic/ Cholinergic Imbalance Hypothesis by comparing GH respo nses to (a) the cholinesterase inhibitor pyridostigmine and (b) the in direct noradrenergic agonist desipramine in a depressed group (n = 9) and a matched control group. The depressed patients fulfilled criteria for DSM-111-R diagnosis of Major Depression: Melancholic Subtype. Thr ee GH challenge tests were administered in each subject: desipramine, pyridostigmine and GH-releasing hormone (GHRH). The latter was perform ed to determine pituitary reserve. Each subject also had a dexamethaso ne suppression test. GH responses (as measured by peak minus baseline values) to GHRH were significantly blunted in the depressed (26.1 +/- 4.9 mU/L) compared to the control group (48.4 +/- 4. 9 m U/L: t = 2.2, df = 16, p < 0.05); and were positively correlated to desipramine/GH responses in both the depressed and control groups (p < 0.001). Peak G H responses to pyridostigmine were relatively increased in the depress ed sample (12.2 +/- 1.8 m U/L Vs 6.9 +/- 1.5 m U/L; t 2.5, df = 16, p < 0.05). Within the depressed group, dexamethasone non-suppressors had blunted GH responses to desipramine compared to those who cortisol su ppressed (p < 0.05). These findings (a) lend some support to the 'Chol inergic/Adrenergic Imbalance Hypothesis', (b) suggest that desipramine may bring about the release of GH via the GHRH pathway and (c) blunti ng of the desipramine/GH response is associated with hypercortisolaemi a.