Copy number variations (CNV) in depression


A large genetic study of people with major depression has found that a duplicated region of DNA on chromosome 5 predisposes people to the disorder. The gene involved plays an important role in the development of nerve cells, adding to evidence that disruptions in neurotransmission networks form a biological basis for depression. [...]

[This study] is the first large-scale genome-wide study of copy number variation (CNV) in major depressive disorder (MDD), a major psychiatric and behavioral disorder affecting an estimated 16 percent of the U.S. population. [...]

Hakonarson’s group conducted a whole-genome scan of DNA from 1,693 patients with MDD, mainly from a European database, and from 4,506 control subjects.

The researchers identified 12 CNVs exclusive to MDD cases. Their most notable finding was a large duplication of DNA segments on chromosome 5q35.1, a CNV shared by five unrelated patients and not observed in healthy controls. Residing at that location is the gene SLIT3, which is involved in axon development. The axon is the portion of a neuron that carries nerve impulses away from the cell body. (via.)

Original source: “Duplication of the SLIT3 Locus on 5q35.1 Predisposes to Major Depressive Disorder,” PLoS One, published online Dec. 1, 2010.


Anabolic steroids, depression, BDNF & morning corticosterone levels


Abuse of anabolic androgenic steroids (AASs) is frequently associated with changes in mood, including depression. [...] We used male adult rats injected for 4 weeks with either nandrolone or stanozolol at daily doses (5 mg/kg, s.c.) that are considered equivalent to those abused by humans [...] AAS treatment reduced levels of brain-derived neurotrophic factor in the hippocampus and prefrontal cortex, reduced the expression of low-affinity glucocorticoid receptors in the hippocampus, and increased morning trough basal plasma corticosterone levels. All these changes have been related to the pathophysiology of major depressive disorder. Accordingly, rats treated with nandrolone or stanozolol showed an increased immobility time in the forced swim test, which is widely used for the screening of antidepressant drugs. All effects produced by AASs were prevented by co-administration with the classical antidepressant, chlorimipramine. (via.)