In principle, bAP-dependent calcium influx can also vary in a branch-specific manner, independent of distance from the soma. Experimentally boosting distal bAP amplitude can restore LTP by amplifying bAP-dependent calcium influx ( Sjöström and Häusser, 2006), suggesting that location-dependent variation in synaptic plasticity rules is primarily determined by the local amplitude and timing of bAP-dependent calcium influx. In distal dendritic compartments, smaller amplitude bAPs evoke less voltage-dependent calcium-influx, such that induction protocols that usually evoke LTP result in LTD ( Nevian and Sakmann, 2006 Sjöström and Häusser, 2006). Location-dependent plasticity rules vary along the proximodistal axis of dendrites because bAPs are attenuated as they propagate away from the soma ( Regehr et al., 1989 Spruston et al., 1995 Golding et al., 2002 Waters et al., 2003 Froemke et al., 2005 Sjöström and Häusser, 2006). Such location-dependent plasticity rules may bolster the integrative capacity of individual neurons by supporting divergent tuning properties in basal and apical dendritic arbors ( Larkum et al., 1999 Xu et al., 2012 Iacaruso et al., 2017). The same protocol can evoke a different sign, magnitude, or temporal profile of synaptic plasticity if applied to synapses in proximal or distal dendritic compartments. However, other studies have shown that the outcome of plasticity induction protocols also depends on the synaptic location within the dendritic tree ( Golding et al., 2002 Froemke et al., 2005 Sjöström and Häusser, 2006 Gordon et al., 2006). Many investigations have focused on timing-dependent plasticity rules, such as spike-timing dependent plasticity (STDP), in which the delay between synaptic input and the bAP determines if an induction protocol results in long-term potentiation (LTP), depression (LTD), or maintenance of synapse strength ( Feldman, 2012). The synaptic tuning properties of neurons are regulated by calcium-dependent plasticity signals, including voltage-dependent calcium influx evoked by back-propagating action potentials (bAPs) ( Magee and Johnston, 1997 Sjöström and Nelson, 2002 Häusser and Mel, 2003). Branch-specific compartmentalization of bAP-dependent calcium signals may provide a mechanism for neurons to diversify synaptic tuning across the dendritic tree. Finally, we show that bAPs still amplify synaptically-mediated calcium influx in these branches because of differences in the voltage-dependence and kinetics of VGCCs and NMDA-type glutamate receptors. We demonstrate that these branches have more elaborate branch structure compared to sister branches, which causes a local reduction in electrotonic impedance and bAP amplitude. These branches contain VGCCs and successfully propagate bAPs in the absence of synaptic input nevertheless, they fail to exhibit bAP-evoked calcium influx due to a branch-specific reduction in bAP amplitude. Here, we reveal that bAPs fail to evoke calcium influx through voltage-gated calcium channels (VGCCs) in a specific population of dendritic branches in mouse cortical layer 2/3 pyramidal cells, despite evoking substantial VGCC-mediated calcium influx in sister branches. However, it is not known if neurons exhibit branch-specific variability in bAP-dependent calcium signals, independent of distance-dependent attenuation. Attenuation of bAP amplitude in distal dendritic compartments alters plasticity in a location-specific manner by reducing bAP-dependent calcium influx. Back-propagating action potentials (bAPs) regulate synaptic plasticity by evoking voltage-dependent calcium influx throughout dendrites.
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