| Autor: |
Theis AK; Neuroscience Research Center, Charité Universitätsmedizin Berlin, Berlin, Germany., Rózsa B; Laboratory of 3D Functional Network and Dendritic Imaging, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.; Faculty of Information Technology and Bionics, Pázmány Péter University, Budapest, Hungary., Katona G; Faculty of Information Technology and Bionics, Pázmány Péter University, Budapest, Hungary., Schmitz D; Neuroscience Research Center, Charité Universitätsmedizin Berlin, Berlin, Germany.; Einstein Center for Neuroscience, Berlin, Germany.; Bernstein Center for Computational Neuroscience, Berlin, Germany.; Cluster of Excellence 'Neurocure', Berlin, Germany.; DZNE-German Center for Neurodegenerative Disease, Berlin, Germany., Johenning FW; Neuroscience Research Center, Charité Universitätsmedizin Berlin, Berlin, Germany.; Einstein Center for Neuroscience, Berlin, Germany.; Berlin Institute of Health (BIH), Berlin, Germany. |
| Abstrakt: |
The majority of excitatory synapses are located on dendritic spines of cortical glutamatergic neurons. In spines, compartmentalized Ca 2+ 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 Ca 2+ channels (VGCCs). For spines, this global mode of spine Ca 2+ 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 Ca 2+ influx. Here, we investigate how spine VGCCs affect glutamatergic synaptic transmission. We combined electrophysiology, two-photon Ca 2+ imaging and two-photon glutamate uncaging in acute brain slices from rats. T- and R-type VGCCs were the dominant depolarization-associated Ca 2+ 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 Ca 2+ influx, the amount of EPSP mediated Ca 2+ 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. |
