Recent experimental results suggest that dendritic and back-propagating spikes can influence synaptic plasticity in different ways [1]. In this study we investigate how these signals could temporally interact at dendrites leading to changing plasticity properties at local synapse clusters. Similar to a previous study [2], we employ a differential Hebbian plasticity rule to emulate spike-timing dependent plasticity. We use dendritic (D-) and back-propagating (BP-) spikes as post-synaptic signals in the learning rule and investigate how their interaction will influence plasticity. We will analyze a situation where synapse plasticity characteristics change in the course of time, depending on the type of post-synaptic activity momentarily elicited. Starting with weak synapses, which only elicit local D-spikes, a slow, unspecific growth process is induced. As soon as the soma begins to spike this process is replaced by fast synaptic changes as the consequence of the much stronger and sharper BP-spike, which now dominates the plasticity rule. This way a winner-take-all-mechanism emerges in a two-stage process, enhancing the best-correlated inputs. These results suggest that synaptic plasticity is a temporal changing process by which the computational properties of dendrites or complete neurons can be substantially augmented.

Recent experimental results suggest that dendritic and back-propagating spikes can influence synaptic plasticity in different ways [1]. In this study we investigate how these signals could temporally interact at dendrites leading to changing plasticity properties at local synapse clusters. Similar to a previous study [2], we employ a differential Hebbian plasticity rule to emulate spike-timing dependent plasticity. We use dendritic (D-) and back-propagating (BP-) spikes as post-synaptic signals in the learning rule and investigate how their interaction will influence plasticity. We will analyze a situation where synapse plasticity characteristics change in the course of time, depending on the type of post-synaptic activity momentarily elicited. Starting with weak synapses, which only elicit local D-spikes, a slow, unspecific growth process is induced. As soon as the soma begins to spike this process is replaced by fast synaptic changes as the consequence of the much stronger and sharper BP-spike, which now dominates the plasticity rule. This way a winner-take-all-mechanism emerges in a two-stage process, enhancing the best-correlated inputs. These results suggest that synaptic plasticity is a temporal changing process by which the computational properties of dendrites or complete neurons can be substantially augmented.

Recent experimental results suggest that dendritic and back-propagating spikes can influence synaptic plasticity in different ways [1]. In this study we investigate how these signals could temporally interact at dendrites leading to changing plasticity properties at local synapse clusters. Similar toa previous study [2], we employ a differential Hebbian plasticity rule to emulate spike-timing dependent plasticity. We use dendritic (D-) and back-propagating (BP-) spikes as post-synaptic signals in the learning ruleand investigate how their interaction will influence plasticity. We will analyze a situation where synapse plasticity characteristics change in the course of time, depending on the type of post-synaptic activity momentarily elicited.Starting with weak synapses, which only elicit local D-spikes, a slow, unspecific growth process is induced. As soon as the soma begins to spike this process is replaced by fast synaptic changes as the consequence of the much stronger and sharper BP-spike, which now dominates the plasticity rule. This way a winner-take-all-mechanism emerges in a two-stage process, enhancing the best-correlated inputs. These results suggest that synaptic plasticity is a temporal changing process bywhich the computational properties of dendrites or complete neurons canbe substantially augmented.

Spike timing plasticity (STDP) is a special form of synaptic plasticity where the relative timing of post-and presynaptic activity determines the change of the synaptic weight. On the postsynaptic side, active backpropagating spikesin dendrites seem to play a crucial role in the induction of spike timing dependent plasticity. We argue that postsynaptically the temporal change of the membrane potential determines the weight change. Coming from the presynaptic side induction of STDP is closely related to the activation of NMDA channels. Therefore, we will calculate analytically the change of the synaptic weight by correlating the derivative ofthe membrane potential with the activity of the NMDA channel.

Spike timing plasticity (STDP) is a special form of synaptic plasticity where the relative timing of post-and presynaptic activity determines the change of the synaptic weight. On the postsynaptic side, active backpropagating spikes in dendrites seem to play a crucial role in the induction of spike timing dependent plasticity. We argue that postsynaptically the temporal change of the membrane potential determines the weight change. Coming from the presynaptic side induction of STDP is closely related to the activation of NMDA channels. Therefore, we will calculate analytically the change of the synaptic weight by correlating the derivative of the membrane potential with the activity of the NMDA channel.

Spike timing plasticity (STDP) is a special form of synaptic plasticity where the relative timing of post-and presynaptic activity determines the change of the synaptic weight. On the postsynaptic side, active backpropagating spikes in dendrites seem to play a crucial role in the induction of spike timing dependent plasticity. We argue that postsynaptically the temporal change of the membrane potential determines the weight change. Coming from the presynaptic side induction of STDP is closely related to the activation of NMDA channels. Therefore, we will calculate analytically the change of the synaptic weight by correlating the derivative of the membrane potential with the activity of the NMDA channel.