βCaMKII in Lateral Habenula Mediates Core Symptoms of Depression

• DOI: 10.1126/science.1240729
• Publication Date: 2013-08-29T18:10:40Z
• Authors: Kun Li; Tao Zhou; Lujian Liao; Zhongfei Yang; Catherine Wong; Fritz Henn; Roberto Malinow; John R. Yates; Hailan Hu
• Keywords: Male; Neurons; Proteomics; 0301 basic medicine; Depressive Disorder, Major; Habenula; 0303 health sciences; Antidepressive Agents; Rats; Mice, Inbred C57BL; Rats, Sprague-Dawley; Disease Models, Animal; Mice; 03 medical and health sciences; Gene Knockdown Techniques; Animals; Humans; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Promoter Regions, Genetic

Depression and the Habenula

The lateral habenula (LHb) appears to have a role in depression. However, the underlying mechanisms are poorly understood, and by using multiple rodent models of depression,

Li et al.

(p. 1016 ) identified a signaling pathway and associated neuronal adaptations in which the enzyme βCaMKII was selectively up-regulated in the LHb. Manipulations that enhanced βCaMKII levels increased depression-related phenotypes, and RNA interference of CaMKIIb blunted depression. Enhanced βCaMKII levels in the habenula promoted excitatory synaptic transmission on these neurons and increased action potential firing mediated by an up-regulation of a specific subtype of glutamate receptors.