Secretion of hormones in the anterior pituitary is under the control, both direct and indirect, of central neuronal cell bodies that may project relatively widely within the brain. The secretion of a given hormone in response to specific precursors or agonists for individual neurotransmitter receptors has been proposed as a way of testing the security of such connections. Hormone secretion provides a bioassay of the system of interest. There is a measure of consensus about the findings in major depression.
Precursor loading of the serotonergic system with intravenous tryptophan produces prolactin and growth hormone secretion. In depressed patients, prolactin and growth hormone responses are blunted but recover with treatment/22) Responses to intravenous clomipramine, which similarly releases 5-HT by a presynaptic mechanism, are also blunted in depression.(23) The receptors mediating these responses are uncertain, although in any case the requirement for an intact presynaptic system precludes interpretation in terms of receptor subtype.
Appropriately selective agonists with full efficacy are not freely available for testing postsynaptic or presynaptic responses. However, buspirone, gepirone, and ipsapirone are all partial agonists at the 5-HT 1A receptor and have been looked at in a preliminary way in depressed patients. There is disagreement about whether postsynaptic (endocrine) responses are or are not blunted, but there is more consensus that presynaptic (hypothermic) responses are blunted. (24)
Noradrenergic and dopaminergic function has been examined using the a (2)-adrenoceptor agonist clonidine and the mixed D1/2 receptor agonist apomorphine. Growth hormone responses to clonidine are usually reported as being blunted in major depression. (25) Apomorphine-stimulated growth hormone responses are also blunted in depressed patients/2.6) while, in symmetry, patients at risk of postpartum psychosis (usually manic in form) have enhanced apomorphine responses. (27)
Cholinergic challenge with an acetylcholinesterase inhibitor such as pyridostigmine or physostigmine produces a secretion of growth hormone; responses in major depression were increased compared with controls.(28)
Neuroendocrine drug challenge suggests attenuated serotonergic function and increased cholinergic function in depression. Reduced responses to adrenergic and dopaminergic challenge also suggest impaired neurotransmission. Interpretation of tests with agonists is always difficult, because blunting may occur in an overactive system that has been downregulated. In addition, if the secretion of the assay hormone itself is actually directly affected by the state of depression, interpretation in terms of specific neurotransmitter abnormalities may be misleading. This is a particular problem for ACTH/cortisol responses (see below). In fact, enthusiasm for neuroendocrine surrogate markers of monoamine transmission within the brain has probably diminished in recent years, but the paradigm of drug challenge nevertheless remains interesting. We must assay brain responses of the monoamine projections more centrally involved in mood regulation.
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