Read on Twitter
My first preprint 
It is a small paper, but probably the one I feel most proud about bc I pulled it off on my own, in the middle of grief and a pandemic. Plus it is about my two favorite neurotopics: stroke and astrocytes. What's about? Thread (level: easy) 
https://twitter.com/biorxivpreprint/status/1341115046424920071
It is a small paper, but probably the one I feel most proud about bc I pulled it off on my own, in the middle of grief and a pandemic. Plus it is about my two favorite neurotopics: stroke and astrocytes. What's about? Thread (level: easy) https://twitter.com/biorxivpreprint/status/1341115046424920071
In our previous paper published in @NeuroCellPress we found that mice lacking the astrocyte protein Chordin like 1 (aka Chrdl1 KO) showed enhanced plasticity. So we thought 
maybe Chrdl1 KO mice could repair their damaged neuronal connections more efficiently after stroke.
maybe Chrdl1 KO mice could repair their damaged neuronal connections more efficiently after stroke.
As it turned out, absence of Chrdl1 doesn't have much influence on a bunch of stroke hallmarks: astrogliosis, microglia activation (sorry if u don't like the term), or injury volume 
But (drum roll 
) absence of Chrdl1 prevents dendritic spine loss, which suggests that Chrdl1 KO 
are protected from synaptic loss in stroke.
) absence of Chrdl1 prevents dendritic spine loss, which suggests that Chrdl1 KO are protected from synaptic loss in stroke.
How does Chrdl1 influence spine density after stroke? Is it through AMPAR regulation? BMP signaling? Is it the same in any brain region after stroke? Follow my lab's future work, time (and experiments 
) will tell.
) will tell.
