Plasticity and function of backpropagating Action Potential mediated calcium signals in dendritic spines
Final Report Abstract
In the project we have identified a neuronal mechanism that may play a role in memory formation. Research findings obtained over the past decades increasingly indicate that stored memories are coded as permanent changes of neuronal communication and the strength of neuronal interconnections. During learning, a specific pattern of neuronal electrical activity induces cellular changes that alter the response to synaptic inputs, the expression of genes and the cellular morphology beyond the learning process itself. The project focused on identifying physiological mechanisms through which a neuron can implement long-term changes of its response. Spines are small dendritic processes that host the majority of excitatory synapses. Whenever a cell fires an action potential, the back-propagating action potential depolarizes the spines. Sufficient spine depolarization opens voltage gated Ca2+ channels. As a result, the rapid influx of calcium ions from the outside changes the spine Ca2+ concentration. In addition, the intracellular ryanodine receptor gets activated by Ca2+ influx, which triggers the release of calcium stored in the endoplasmic reticulum of the cell. We demonstrate that the voltage gated Ca2+ channel mediated spine calcium response to action potentials backpropagating into the dendritic tree can undergo long-term enhancement. Functionally, induction of this enhancement occurs in a ryanodine receptor nano-domain. It should be noted that these changes are limited to individual spines - neighboring spines remain unaffected. Our next aim was to understand what influence these spine-specific, long-term, altered calcium responses exert on the synaptic communication between the neurons. Our current conclusion is that spine voltage gated Ca2+ channels activated by backpropagating action potentials are functionally uncoupled from fast, AMPA-type glutamate receptor mediated baseline synaptic transmission. In the future, we want to test whether enhanced backpropagating action potential mediated spine Ca2+ signals play a role in metaplasticity.
Publications
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A Calcium-Dependent Mechanism of Neuronal Memory [editorial synopsis]. PLOS Biology, June 22, 2015
Gasque, G
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Ryanodine Receptor Activation induces Long-Term Plasticity of Spine Calcium Dynamics. PLOS Biology, June 22, 2015
Johenning, F.W., Theis, A., Pannasch, U., Rückl, M., Rüdiger, S., Schmitz, D.
