This study is designed to identify whether indices of possible noradrenergic dysfunction in depression are either """"""""state"""""""" or """"""""trait"""""""" markers. Trait markers would be expected to be abnormal in both acute and remitted depressed patients and thus be consistent across states. State markers would be expected to be abnormal in acute, but not remitted, depressed patients and thus not be consistent across states. This study focuses on 1) indices of noradrenergic release and metabolism such as plasma norepinephrine and 3-methoxy-4-hydroxyphenylglycol (MHPG) and 2) indices of adrenergic receptors responsiveness, i.e., measures that depend on the responsiveness of central adrenergic receptors, such as the growth hormone (GH) and plasma MHPG response to the Alpha2-adrenergic agonist, clonidine. Preliminary evidence raises the possibility that an abnormal, blunted GH response to clonidine is a trait marker for depression, i.e., it persists in unmedicated remitted patients. In contrast, some evidence suggests that measures of noradrenergic release and metabolism are state-related or inconsistent across states. The specific objectives of this study are to evaluate two basal indices of noradrenergic release and metabolism: plasma MHPG and NE, as well as several indices of Alpha2-adrenergic receptor responsiveness as reflected in the GH, MHPG, NE, and heart rate responses to clonidine in medication-free depressed patients in both the acute and remitted states. In a within-subjects design, a single cohort of depressed patients studied in both the acute and remitted state will be compared for consistency of these indices across states. In a between-subjects design, these indices in both remitted and acute patients will be respectively compared to matched controls. It is hypothesized that while abnormalities in basal concentrations of plasma MHPG and NE will be observed only in the acute state, the GH and plasma MHPG responses to clonidine will be abnormal in both acute and remitted patients compared to controls and that these abnormal responses to clonidine within a single cohort of patients will be consistent across states.
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