Deans' stroke musings: Microglia Promote Learning-Dependent Synapse Formation through Brain-Derived Neurotrophic Factor

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, December 23, 2013

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 Gan send email

See 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.