Mammalian dendrites are active structures capable of regenerative electrical activity. Using fast confocal imaging in combination with low affinity calcium indicator dyes and voltage imaging we have investigated the characteristics and physiological function of local dendritic spikes in layer 5 pyramidal neurons of mouse visual cortex.

We found that these dendritic spikes initiate a fast calcium transient in a small spine-dendritic compartment. Furthermore, a single of these dendritic spikes induced long-term synaptic depression (sLTD). This form of activity-dependent synaptic plasticity did not require somatic spiking. The induction of sLTD is input-specific and dependent on activation of NMDA-receptors. However, the co-incident activation of a single synaptically-induced local dendritic spike and a back-propagating action potential often produced long-term potentiation (sLTP). We found a tight correlation between the amplitude of the dendritic calcium transient during induction and the direction of the resulting synaptic plasticity. A low amplitude calcium transient in the spine-dendritic compartment induced sLTD, whereas a high amplitude calcium transient induced sLTP. Experiments using moderate intracellular BAPTA concentrations revealed that the calcium transients in activated spines are crucial for the induction of single shock synaptic plasticity. There was a strong correlation between the amplitude of the calcium transients in activated spines and the direction of the resulting synaptic plasticity. A low amplitude calcium transient in the activated spines induced sLTD, whereas a high amplitude calcium transient induced sLTP.

In conclusion, we identified a new form of rapidly induced bidirectional synaptic plasticity. We propose that sLTP and sLTD underlie the rapid acquisition of information in cortical circuits.