A Potential Contribution of Chemokine Network Dysfunction to the Depressive Disorders

Author(s): Joanna Ślusarczyk, Ewa Trojan, Jakub Chwastek, Katarzyna Głombik, Agnieszka Basta-Kaim

Journal Name: Current Neuropharmacology

Volume 14 , Issue 7 , 2016

Become EABM
Become Reviewer
Call for Editor

Graphical Abstract:


In spite of many years of research, the pathomechanism of depression has not yet been elucidated. Among many hypotheses, the immune theory has generated a substantial interest. Up till now, it has been thought that depression is accompanied by the activation of inflammatory response and increase in pro-inflammatory cytokine levels. However, recently this view has become controversial, mainly due to the family of small proteins called chemokines. They play a key role in the modulation of peripheral function of the immune system by controlling immune reactions, mediating immune cell communication, and regulating chemotaxis and cell adhesion. Last studies underline significance of chemokines in the central nervous system, not only in the neuromodulation but also in the regulation of neurodevelopmental processes, neuroendocrine functions and in mediating the action of classical neurotransmitters. Moreover, it was demonstrated that these proteins are responsible for maintaining interactions between neuronal and glial cells both in the developing and adult brain also in the course of diseases.

This review outlines the role of chemokine in the central nervous system under physiological and pathological conditions and their involvement in processes underlying depressive disorder. It summarizes the most important data from experimental and clinical studies.

Keywords: Antidepressant drugs, chemokine, chemokine receptors, depression, neuroinflammation, neuroplasticity, neuroendocrinology, neurotransmission.

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2016
Published on: 19 February, 2016
Page: [705 - 720]
Pages: 16
DOI: 10.2174/1570159X14666160219131357
Price: $65

Article Metrics

PDF: 27
PRC: 1