Phosphorylation and Synaptic Plasticity
Professor Tom O'Dell comments that phosphorylation plays a crucial role in synaptic plasticity.
Phosphorylation has a crucial role in synaptic plasticity. Synaptic plasticity, of course, is the ability of different patterns of activity at a synapse to modify the synapse â€“ to make it stronger or weaker. And we now that a key component of that process, the process that makes synapses work better or work not as well, is due to changes in phosphorylation â€“ particularly of the glutamate receptors, the neurotransmitter receptors that detect the chemical signals that are released from the presynaptic cell. Phosphorylation of those proteins changes the strength of synaptic transmission changes.
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Professor Tom O'Dell defines depotentiation - the erasure of long-term potentiation (LTP) at the synapse.
Professor Tom O'Dell discusses synaptic plasticity - the strengthening and weakening of synaptic connections between neurons.
Professor Tom O'Dell describes the role played by NMDA receptors, as part of a large multi-protein complex, in facilitating long-term potentiation (LTP).
Professor Tom O'Dell defines phosphorylation - the addition of a phosphate group to a protein molecule to regulate gene function.
Professor Tom O'Dell discusses the importance of electrophysiology to the study of cognition.
Professor Graham Collingridge describes the glutamate receptor, AMPA, the workhorse receptor for communicating information.
Cognitive information is encoded in patterns of nervous activity and decoded by molecular listening devices at the synapse. Professor Seth Grant explains how different patterns of neural firing are critical to cognition.
It is increasingly clear that the nonneuronal brain cells called glia are intricately involved in the neuronal crosstalk at synapses.
Professor Tom O'Dell describes different techniques for studying the physiology of the nervous system.
Professor Tom O'Dell introduces some of the advanced techniques used to examine the electrical activity of brain cells.