scholarly journals Cell Type-Specific Loss of BDNF Signaling Mimics Optogenetic Control of Cocaine Reward

Science ◽  
2010 ◽  
Vol 330 (6002) ◽  
pp. 385-390 ◽  
Author(s):  
M. K. Lobo ◽  
H. E. Covington ◽  
D. Chaudhury ◽  
A. K. Friedman ◽  
H. Sun ◽  
...  
2020 ◽  
Vol 219 (7) ◽  
Author(s):  
Katy L.H. Marshall-Phelps ◽  
Linde Kegel ◽  
Marion Baraban ◽  
Torben Ruhwedel ◽  
Rafael G. Almeida ◽  
...  

Through a genetic screen in zebrafish, we identified a mutant with disruption to myelin in both the CNS and PNS caused by a mutation in a previously uncharacterized gene, slc12a2b, predicted to encode a Na+, K+, and Cl− (NKCC) cotransporter, NKCC1b. slc12a2b/NKCC1b mutants exhibited a severe and progressive pathology in the PNS, characterized by dysmyelination and swelling of the periaxonal space at the axon–myelin interface. Cell-type–specific loss of slc12a2b/NKCC1b in either neurons or myelinating Schwann cells recapitulated these pathologies. Given that NKCC1 is critical for ion homeostasis, we asked whether the disruption to myelinated axons in slc12a2b/NKCC1b mutants is affected by neuronal activity. Strikingly, we found that blocking neuronal activity completely prevented and could even rescue the pathology in slc12a2b/NKCC1b mutants. Together, our data indicate that NKCC1b is required to maintain neuronal activity–related solute homeostasis at the axon–myelin interface, and the integrity of myelinated axons.


2005 ◽  
Vol 93 (4) ◽  
pp. 1000-1009 ◽  
Author(s):  
M. Malanga ◽  
M. Romano ◽  
A. Ferone ◽  
A. Petrella ◽  
G. Monti ◽  
...  

2014 ◽  
Vol 76 (10) ◽  
pp. 794-801 ◽  
Author(s):  
Margarita Arango-Lievano ◽  
Justin T. Schwarz ◽  
Mary Vernov ◽  
Matthew B. Wilkinson ◽  
Kathryn Bradbury ◽  
...  

2019 ◽  
Vol 39 (24) ◽  
pp. 4657-4667 ◽  
Author(s):  
Puja K. Parekh ◽  
Ryan W. Logan ◽  
Kyle D. Ketchesin ◽  
Darius Becker-Krail ◽  
Micah A. Shelton ◽  
...  

2017 ◽  
Vol 55 (05) ◽  
pp. e28-e56
Author(s):  
S Macheiner ◽  
R Gerner ◽  
A Pfister ◽  
A Moschen ◽  
H Tilg

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