Clinical and biochemical aspects of depressive disorders: I. Introduction, classification, and research techniques

Abstract

The present review focuses on recent data from clinical and animal research concerning the biochemical bases of depressive disorders, diagnosis, and treatment. In addition to integrating these data, problems and future directions in this research are discussed. The review is presented in three parts. This study, Part I, describes diagnostic classification schemes for depressive disorders, some epidemiological and biological correlates of the classifications, and research techniques for investigating depressive disorders. Research techniques include animal models, human biochemical techniques, and Positron Emission Tomography. In a future issue, Part II will discuss various transmitter/receptor theories of depressive disorders, e.g., noradrenergic, serotonergic, cholinergic, and dopaminergic, GABAergic, and peptidergic theories. Also in a future issue, Part III will discuss treatments for depression and some of the controversies in the field.

Clinical and biochemical aspects of depressive disorders: III. Treatment and controversies

“…Those that do exist include animals that are genetically bred to have behaviors similar to depressive symptoms. For example, the FSL rat model of depression displays reduced locomotion, supersensitivity to the behavioral depressant and endocrine effects of cholinergic agonists, and reduced REM sleep latencies, similar to some human depressed states (Overstreet, 1986; also see Overstreet and Janowsky section in Part I1 of the present review, Caldecott-Hazard et al, 1991b). In the rat model, the hypothesized biochemical mediators of these behaviors, acetylcholine and dopamine, are, like the behaviors, perpetually altered.…”

“…Part I (Caldecott-Hazard et al, 1991a) described classification schemes for clinical symptoms of depressive disorder, epidemiological and biological correlates of the clinical classifications, and techniques for studying biochemical changes in depressed humans or in animal models. It was hypothesized that the best basis for clinical classification will ultimately derive from proven etiologies and biological mechanisms that underlie depressive disorders.…”

“…Drs. Overstreet and Janowsky addressed this question under cholinergic and catecholaminergic interactions in Part I1 of this review article (Caldecott-Hazard et al, 1991b). They described a shift in opinion from a role for norepinephrine to a role for dopamine in motor activity.…”

“…Still, even within these systems, secondary types of transmitters are probably involved. Neurotransmitter systems influence one another in many ways, as discussed in the sections of this review (Part 11) on noradrenergiclserotonergic interactions (Caldecott-Hazard et al, 1991b) or cholinergidcatecholaminergic interactions (Overstreet and Janowsky, section in Caldecott-Hazard et al, 1991b). This fact is most apparent in the biochemical and physiological effects of antidepressant drugs on the brain.…”

“…Several monkey models of anxiety or depression also display biochemical or physiological changes that are sustained over the animal's lives, and hence may be trait markers of behavior (see section by Kling and Kling in Part I of this review, Caldecott-Hazard et al, 1991a). For example, adult monkeys who had been separated from their mothers early in life were more susceptible to the depressogenic effects of AMPT than control monkeys (Kraemer and McKinney, 1979).…”