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The intersections of NMDAR-dependent synaptic plasticity and cell survival
Thomas E Bartlett1, Yu Tian Wang
1Brain Research Centre, Room F270, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC V6T 2B5, Canada.
Neuropharmacology
|January 30, 2013
Summary
N-methyl D-aspartate receptor (NMDAR) activation is crucial for synaptic plasticity and neuronal survival. This review explores shared mechanisms between NMDAR-dependent plasticity and cell fate, suggesting neuroprotection strategies.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- N-methyl D-aspartate receptors (NMDARs) are critical for synaptic plasticity, particularly long-term potentiation (LTP).
- NMDAR activation also plays a significant role in regulating neuronal death and survival pathways.
- A gap exists in correlating these two vital research areas.
Purpose of the Study:
- To review and correlate the mechanisms of NMDAR-dependent synaptic plasticity with neuronal survival and death.
- To compare these mechanisms with proneurotrophin/neurotrophin receptor and intracellular signaling systems.
- To identify potential novel avenues for neuroprotection.
Main Methods:
- Literature review and synthesis of existing research on NMDAR function.
- Comparative analysis of molecular pathways involved in synaptic plasticity and cell fate.
- Examination of signaling systems, including neurotrophin receptors.
Main Results:
- NMDAR-dependent long-term potentiation (LTP) and long-term depression (LTD) share common molecular mechanisms with neuronal cell survival and cell death, respectively.
- Specific signaling pathways and receptor systems show overlap between plasticity and cell survival/death.
- The interplay between synaptic plasticity and cell survival pathways is highlighted.
Conclusions:
- NMDAR-dependent synaptic plasticity and neuronal cell fate are intricately linked through shared molecular mechanisms.
- The intersection of plasticity and cell survival pathways offers promising targets for neuroprotective therapies.
- Further research into these shared mechanisms could lead to novel treatments for neurological disorders.
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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