Neurobiology of depression

Eric J. Nestler, Michel Barrot, Ralph J. DiLeone, Amelia J. Eisch, Stephen J. Gold, Lisa M. Monteggia

Research output: Contribution to journalReview articlepeer-review

2707 Scopus citations

Abstract

Current treatments for depression are inadequate for many individuals, and progress in understanding the neurobiology of depression is slow. Several promising hypotheses of depression and antidepressant action have been formulated recently. These hypotheses are based largely on dysregulation of the hypothalamic-pituitary-adrenal axis and hippocampus and implicate corticotropin-releasing factor, glucocorticoids, brain-derived neurotrophic factor, and CREB. Recent work has looked beyond hippocampus to other brain areas that are also likely involved. For example, nucleus accumbens, amygdala, and certain hypothalamic nuclei are critical in regulating motivation, eating, sleeping, energy level, circadian rhythm, and responses to rewarding and aversive stimuli, which are all abnormal in depressed patients. A neurobiologic understanding of depression also requires identification of the genes that make individuals vulnerable or resistant to the syndrome. These advances will fundamentally improve the treatment and prevention of depression.

Original languageEnglish
Pages (from-to)13-25
Number of pages13
JournalNeuron
Volume34
Issue number1
DOIs
StatePublished - 28 Mar 2002
Externally publishedYes

Fingerprint

Dive into the research topics of 'Neurobiology of depression'. Together they form a unique fingerprint.

Cite this