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.
