Microglia Promote Learning-Dependent Synapse Formation through Brain-Derived Neurotrophic Factor

No clue what this means but it sounds damned important. So ask your doctor when this will be translated into a stroke protocol. And get in your doctors face until they answer. They are supposed to know more than you do. Hah!
http://www.cell.com/retrieve/pii/S0092867413014815

Cell, Volume 155, Issue 7, 1596-1609, 19 December 2013
Copyright © 2013 Elsevier Inc. All rights reserved.
10.1016/j.cell.2013.11.030

Authors

Christopher N. Parkhurst, Guang Yang, Ipe Ninan, Jeffrey N. Savas, John R. Yates, Juan J. Lafaille, Barbara L. Hempstead, Dan R. Littman, Wen-Biao GanSee Affiliations

• Highlights
• CX₃CR1^CreER mice allow for the specific manipulation of microglial function
• Microglia are important for learning and learning-dependent synaptic remodeling
• Microglial BDNF is an important regulator of synaptic plasticity and function

Summary

Microglia are the resident macrophages of the CNS, and their functions have been extensively studied in various brain pathologies. The physiological roles of microglia in brain plasticity and function, however, remain unclear. To address this question, we generated CX₃CR1^CreER mice expressing tamoxifen-inducible Cre recombinase that allow for specific manipulation of gene function in microglia. Using CX₃CR1^CreER to drive diphtheria toxin receptor expression in microglia, we found that microglia could be specifically depleted from the brain upon diphtheria toxin administration. Mice depleted of microglia showed deficits in multiple learning tasks and a significant reduction in motor-learning-dependent synapse formation. Furthermore, Cre-dependent removal of brain-derived neurotrophic factor (BDNF) from microglia largely recapitulated the effects of microglia depletion. Microglial BDNF increases neuronal tropomyosin-related kinase receptor B phosphorylation, a key mediator of synaptic plasticity. Together, our findings reveal that microglia serve important physiological functions in learning and memory by promoting learning-related synapse formation through BDNF signaling.