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Printable Handouts
Navigable Slide Index
- Introduction
- Ionotropic glutamate receptor subunits
- Long-term potentiation and long-term depression
- An excitatory synapse-low frequency transmission
- AMPARs mediate fast synaptic transmission
- NMDARs' role in low frequency transmission
- NMDARs trigger the induction of LTP
- Synaptic activation of NMDARs
- NMDARs in Mg2+-free media
- Dual component EPSCs
- NMDAR activation in high frequency transmission
- Regulation of an excitatory synapse (1)
- GABAA receptor-mediated synaptic inhibition
- Regulation of an excitatory synapse (2)
- GABAB autoreceptors regulate synaptic inhibition
- Regulation of an excitatory synapse (3)
- GABAB autoreceptors regulate LTP induction
- NMDARs generate local Ca2+ signal in spines (1)
- NMDARs generate local Ca2+ signal in spines (2)
- Ca2+ activates various kinases (including CamKII)
- Possible loci of expression
- Alterations in release properties
- LTP & AMPAR-mediated synaptic transmission
- LTP & NMDAR-mediated synaptic transmission
- Increase in AMPAR function in LTP
- Increase in AMPAR single channel conductance
- Increase in AMPAR number in LTP
- NSF stabilises AMPARs & maintains LTP
- PKMzeta stabilises NSF interaction with AMPARs
- A summary of NMDAR-LTP mechanisms
Topics Covered
- Synaptic plasticity
- Long-term potentiation (LTP)
- Glutamate receptors
- AMPA and NMDA receptors
- Hippocampus
- Learning & Memory
- Phosphorylation
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Talk Citation
Collingridge, G. (2011, October 27). Glutamate receptor modulation and long-term synaptic plasticity [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved February 17, 2019, from https://hstalks.com/bs/2133/.Publication History
Glutamate receptor modulation and long-term synaptic plasticity
Published on October 27, 2011
33 min