This paper describes a hypothesis that attempts to account for how changes in noradrenergic systems in the brain can affect depression-related behaviors and symptoms. It is hypothesized that increased activity of the locus coeruleus (LC) neurons, the principal norepinephrine (NE)-containing cells in the brain, causes release of galanin (GAL) in the ventral tegmentum (VTA) from LC axon terminals in which GAL is colocalized with NE. It is proposed that GAL release in VTA inhibits the activity of dopaminergic cell bodies in this region whose axons project to forebrain, thereby resulting in two of the principal symptoms seen in depression, decreased motor activation and decreased appreciation of pleasurable stimuli (anhedonia). The genesis of this hypothesis, which derives from studies using an animal model of depression, is described as well as recent data consistent with the hypothesis. The formulation proposed suggests that GAL antagonists may be of therapeutic benefit in the treatment of depression.

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Doing scientific research benefits undergraduates, but relatively few research mentors are available. Using stratified random assignment of students to conditions, this study shows that a collaborative learning model produces student outcomes just as positive as a traditional apprenticeship.

A hypothesis is presented that attempts to describe the mechanism by which noradrenergic neurons in the brain influence dopaminergic neurons to produce behavioral changes seen in depression. The historical background pointing to a norepinephrine (NE)‐dopamine (DA) interaction in depression is described. This interaction is suggested by numerous observations indicating that whereas NE is important in therapy and pathogenesis of depression, basic research implicates DA in depression‐related behavioral responses (motor activity changes, hedonic response) much more so than NE. The hypothesized NE‐DA interaction is introduced in relation to an animal model (stress‐induced behavioral depression) that has traced depressive symptomatology to abnormal activity (hyperresponsivity) of locus coeruleus (LC) neurons. Based on recent data by Grenhoff et al. (1993; J Neural Transm 93:11–25), it is suggested that the augmented burst firing of LC neurons found in behavioral depression releases galanin from LC axon terminals, and this inhibits (hyper‐polarizes) DA neurons in the ventral tegmentum (VTA) to mediate depression‐related behavioral changes. Initial results showing that microinfusion of galanin into the VTA decreases spontaneous and swim‐test motor activity of animals are described. Depression 3:225–245 (1995/1996). © 1996 Wiley‐Liss, Inc.

In the present study, we examine immunological functioning in normal healthy African-American and Latino/Latina adolescents recruited from an inner-city high school and an inner-city clinic. A battery of tests was performed with enumerative and functional measures which encompassed both innate and adaptive immunity. We found immune differences related to age, gender, and race on both the enumerative and the functional immune measures. This data expands the available body of information concerning normal immunity in healthy adolescents.