Bidirectional Plasticity Induced By Somatic Integration Of Temporally Correlated EPSPs Initiated At Different Dendrites

Spike timing dependent plasticity (STDP) is a biological process that adjusts thestrength of connections between neurons in the brain. Beyond the traditionalcorrelation-based Hebbian plasticity, STDP opens up new avenes for understandinginformation coding and circuit plasticity that depend on time window which isdefined as the temporal order of pre-and postsynaptic spiking. The classical view ofSTDP is that pairing a single AP with a single EPSP (excitory postsynaptic potential)induces LTP (long-term potentiation) at positive spike timings (EPSP beforepostsynaptic AP) and LTD (long-term depression) at negative spike timings (EPSPafter postsynapt postsynaptic AP).The interaction of two EPSPs within different time windows is a extension ofSTDP. Here we observe that both LTP and LTD can be induced by pairing with twoEPSPs separately initiated at different dendrites of hippocampal CA1pyramidalneurons. LTP can be induced when EPSPs initiated at basal dendrites are before theones initiated at apical dendrites, otherwise when EPSPs initiated at apical dendritesare before the ones initiated at basal dendrites LTD can be induced. Unlike traditionalsynaptic plasticity, such plasticity depends on the soma of pyramidal neurons ratherthan synapses.N-methyl-D-aspartate receptors (NMDARs) are involved in the induction ofsuch bidirectional plasticity. However, such NMDARs target somatic or perisomaticand may be extrasynaptic receptors. Moreover, voltage dependent calciumchannels (VDCCs) are also involved in such bidirectional plasticity. Calcium influxthrough VDCCs is necessary for LTD, but not for LTP.EPSP is a basic excitatory input in the neuron. Exploring the interaction of EPSPs is of great significance. The plasticity induced by the interaction of EPSPsbresks the traditional theory that backpropagation action potential (BAP) or dendriticspike is required for the induction of plasticity. It also challenge the classical viewthat synapses are important for plasticity.Based on our results, in CA1pyramidal neurons bidirectional plasticity may beinduced by the integration of sensory information arriving at apical and basaldendrites. Such integration is different from the signal filtering by BAP in triditiondalsynaptic plasticity, it is a kind of cooperation for the neural signals in hippocampalcircuits. We suggest that the above-mentioned bidirectional plasticity may contributeto the identification and filtering of signals in vivo. When two signals are relevant,they show synergistic growth. However, when two signals are not relevant, both ofthem gradually decrease.