Voltage Gated Calcium Channel Activation by Backpropagating Action Potentials Downregulates NMDAR Function
| Autor: | Theis, Anne-Kathrin, Rózsa, Balázs, Katona, Gergely, Schmitz, Dietmar, Johenning, Friedrich W. |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
calcium
dendritic spines voltage gated Ca2+ channels (VGCCs) NMDAR homeostatic synaptic plasticity synaptic transmission two-photon microscopy ddc:610 Function and Dysfunction of the Nervous System metaplasticity 600 Technik Medizin angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit Neuroscience Original Research |
| Zdroj: | Frontiers in cellular neuroscience 12, 109 (2018). doi:10.3389/fncel.2018.00109 Frontiers in Cellular Neuroscience |
| DOI: | 10.3389/fncel.2018.00109 |
| Popis: | The majority of excitatory synapses are located on dendritic spines of cortical glutamatergic neurons. In spines, compartmentalized Ca2+ signals transduce electrical activity into specific long-term biochemical and structural changes. Action potentials (APs) propagate back into the dendritic tree and activate voltage gated Ca2+ channels (VGCCs). For spines, this global mode of spine Ca2+ signaling is a direct biochemical feedback of suprathreshold neuronal activity. We previously demonstrated that backpropagating action potentials (bAPs) result in long-term enhancement of spine VGCCs. This activity-dependent VGCC plasticity results in a large interspine variability of VGCC Ca2+ influx. Here, we investigate how spine VGCCs affect glutamatergic synaptic transmission. We combined electrophysiology, two-photon Ca2+ imaging and two-photon glutamate uncaging in acute brain slices from rats. T-and R-type VGCCs were the dominant depolarization-associated Ca2+ C conductances in dendritic spines of excitatory layer 2 neurons and do not affect synaptic excitatory postsynaptic potentials (EPSPs) measured at the soma. Using two-photon glutamate uncaging, we compared the properties of glutamatergic synapses of single spines that express different levels of VGCCs. While VGCCs contributed to EPSP mediated Ca2+ influx, the amount of EPSP mediated Ca2+ influx is not determined by spine VGCC expression. On a longer timescale, the activation of VGCCs by bAP bursts results in downregulation of spine NMDAR function. |
| Databáze: | OpenAIRE |
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