scholarly journals Rescue of NMDAR-Dependent Synaptic Plasticity in Fmr1 Knock-Out Mice

2013 ◽  
Vol 25 (1) ◽  
pp. 271-279 ◽  
Author(s):  
C. A. Bostrom ◽  
N.- M. Majaess ◽  
K. Morch ◽  
E. White ◽  
B. D. Eadie ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Knock Out ◽  
Knock Out Mice

scholarly journals Calpain-1 and Calpain-2 in the Brain: New Evidence for a Critical Role of Calpain-2 in Neuronal Death

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2698
Author(s):  
Yubin Wang ◽  
Yan Liu ◽  
Xiaoning Bi ◽  
Michel Baudry
Keyword(s):  
Synaptic Plasticity ◽  
Critical Role ◽  
Protein Targets ◽  
Knock Out ◽  
Regulatory Pathways ◽  
Calcium Dependent ◽  
Binding Domains ◽  
Calpain 2 ◽  
Knock Out Mice ◽  
The Brain

Calpains are a family of soluble calcium-dependent proteases that are involved in multiple regulatory pathways. Our laboratory has focused on the understanding of the functions of two ubiquitous calpain isoforms, calpain-1 and calpain-2, in the brain. Results obtained over the last 30 years led to the remarkable conclusion that these two calpain isoforms exhibit opposite functions in the brain. Calpain-1 activation is required for certain forms of synaptic plasticity and corresponding types of learning and memory, while calpain-2 activation limits the extent of plasticity and learning. Calpain-1 is neuroprotective both during postnatal development and in adulthood, while calpain-2 is neurodegenerative. Several key protein targets participating in these opposite functions have been identified and linked to known pathways involved in synaptic plasticity and neuroprotection/neurodegeneration. We have proposed the hypothesis that the existence of different PDZ (PSD-95, DLG and ZO-1) binding domains in the C-terminal of calpain-1 and calpain-2 is responsible for their association with different signaling pathways and thereby their different functions. Results with calpain-2 knock-out mice or with mice treated with a selective calpain-2 inhibitor indicate that calpain-2 is a potential therapeutic target in various forms of neurodegeneration, including traumatic brain injury and repeated concussions.

scholarly journals Alterations of Endocannabinoid Signaling, Synaptic Plasticity, Learning, and Memory in Monoacylglycerol Lipase Knock-out Mice

2011 ◽  
Vol 31 (38) ◽  
pp. 13420-13430 ◽  
Author(s):  
B. Pan ◽  
W. Wang ◽  
P. Zhong ◽  
J. L. Blankman ◽  
B. F. Cravatt ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Monoacylglycerol Lipase ◽  
Knock Out ◽  
Knock Out Mice

Increased glyoxalase-1 levels in Fkbp5 knock-out mice caused by Glo1 gene duplication

2013 ◽  
Vol 46 (06) ◽  
Author(s):  
LK Kollmannsberger ◽  
NC Gassen ◽  
A Bultmann ◽  
J Hartmann ◽  
P Weber ◽  
...  
Keyword(s):  
Gene Duplication ◽  
Knock Out ◽  
Glyoxalase 1 ◽  
Knock Out Mice
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