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Item Type: | Article |
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Title: | Voltage gated calcium channel activation by backpropagating action potentials downregulates NMDAR function |
Creators Name: | Theis, A.K., Rózsa, B., Katona, G., Schmitz, D. and Johenning, F.W. |
Abstract: | 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+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. |
Keywords: | Dendritic Spines, Two-Photon Microscopy, Calcium, Synaptic Transmission, Voltage Gated Ca2+ Channels (VGCCs), Metaplasticity, Homeostatic Synaptic Plasticity, NMDAR, Animals, Rats |
Source: | Frontiers in Cellular Neuroscience |
ISSN: | 1662-5102 |
Publisher: | Frontiers Media SA |
Volume: | 12 |
Page Range: | 109 |
Date: | 23 April 2018 |
Official Publication: | https://doi.org/10.3389/fncel.2018.00109 |
PubMed: | View item in PubMed |
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