Abstract
Caspases are a family of cysteine proteases that play key roles in programmed cell death (apoptosis). Mounting evidence in recent years shows that caspases also have important non-apoptotic functions in multiple cellular processes, such as synaptic plasticity, dendritic development, learning and memory. In this article, we review the studies on the non-apoptotic functions of caspases in neurons, with a focus on their roles in synaptic plasticity, learning and memory and neurodegeneration.
Highlights
Caspases are a family of cysteine proteases that have a conserved cysteine residue at their active site and cleave after an aspartate residue in their substrates
We recently reported that caspase-3 and the mitochondrial pathway of apoptosis play a critical role in long-term depression (LTD)
The spatial and temporal properties of mitochondrial activation in LTD are still unclear, we found that mitochondria can be very close to synapses, and their morphology, distribution and motility are regulated by synaptic stimulation [33]
Summary
Caspases are a family of cysteine proteases that have a conserved cysteine residue at their active site and cleave after an aspartate residue in their substrates. In Tg2576 transgenic mice that express mutant human amyloid precursor protein, caspase-3 activity is enhanced in dendritic spines roughly coincident with the onset of memory decline and in the apparent absence of neuronal cell death in these animals [45]. Analysis of synaptic functions in the Tg2576 mice suggests that caspase activation leads to dephosphorylation and removal of AMPA receptor subunit GluA1 from synapses (possibly by activating calcineurin), altered glutamatergic synaptic transmission, and enhanced LTD in hippocampal CA1 neurons [45]. These studies suggest that abnormally active caspases may contribute to synaptic deficits in the AD brain, even before frank neuronal death. It is intriguing that injection of caspase-3 inhibitor into the Tg2576 transgenic mice ameliorates the memory defects [45]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
