The Scope of Depression.- The Epidemiology of Bipolar and Nonbipolar Depression: Rates and Risks.- Depression and Affective Disorder in Later Life.- Gender and Depression.- Recent Life Events and Depression.- Vulnerability to Depression: The Lack of Social Support Does Not Cause Depression.- Stress, Conflict, and Depression.- Separation Models and Depression.- Learned Helplessness - An Animal Model Revisited.- Neurobiologic Dimensions of Depression and Mania.- Current Status of Genetic Research in Affective Disorders.- Neuroendocrine Function in Depression.- Opioid Systems and the Regulation of Mood: Possible Significance in Depression?.- Neurophysiologic Studies of Depression: State of the Art.- Chronobiology of Depression.- New Research Techniques for Studying the Functional Anatomy of Depression.- Depression and Altered Neurotransmission - States, Traits, and Interactions.- Pharmacological Models of Depression.- Heuristically Important Mood-altering Drugs.- Mode of Action of Antidepressant Drugs - Primary Effects.- Mode of Action of Antidepressant Agents and ECT - Adaptive Changes After Subchronic Treatment.- Risk Factors Group Report.- Animal Models Group Report.- Functional Indices of Biological Disturbance Group Report.- Neurotransmission Group Report.- List of Participants.- Author Index.

3 and a fraction mayor may not respond to treatment. On the behavioral level, animal research shows that a variety of experimental conditions can induce de­ pression. The same is true in the field of treatment, where pharmacologically highly different drugs can equally alleviate depression in animals and hu­ mans. The question as to whether this is due to a heterogeneity of depressive subjects based on different pathogenetic mechanisms is open to discussion. We can look for common features of all possible causal factors in the hope of finding a single basic mechanism. Many divergent findings may also be ex­ plained as peripheral changes of a highly complicated dynamic system. In the field of psychopharmacology, a circular reasoning has become evident in the sense that originally the clinical antidepressive response was founded on empirical grounds only. In a second step, an attempt was made to characterize some clinically active compounds pharmacologically, and in a third, further compounds were developed based on aspects of the pharmaco­ logical profiles. Moreover, the post hoc development of a pharmacological screening method has the serious disadvantage of delaying breakthroughs into new fields.