Spike Timing Dependent Plasticity Finds the Start of Repeating Patterns in Continuous Spike Trains

Experimental studies have observed Long Term synaptic Potentiation (LTP) when a presynaptic neuron fires shortly before a postsynaptic neuron, and Long Term Depression (LTD) when the presynaptic neuron fires shortly after, a phenomenon known as Spike Timing Dependant Plasticity (STDP). When a neuron is presented successively with discrete volleys of input spikes STDP has been shown to learn ‘early spike patterns’, that is to concentrate synaptic weights on afferents that consistently fire early, with the result that the postsynaptic spike latency decreases, until it reaches a minimal and stable value. Here, we show that these results still stand in a continuous regime where afferents fire continuously with a constant population rate. As such, STDP is able to solve a very difficult computational problem: to localize a repeating spatio-temporal spike pattern embedded in equally dense ‘distractor’ spike trains. STDP thus enables some form of temporal coding, even in the absence of an explicit time reference. Given that the mechanism exposed here is simple and cheap it is hard to believe that the brain did not evolve to use it

Experimental and computational aspects of signaling mechanisms of spike-timing-dependent plasticity

STDP (spike-timing-dependent synaptic plasticity) is thought to be a synaptic learning rule that embeds spike-timing information into a specific pattern of synaptic strengths in neuronal circuits, resulting in a memory. STDP consists of bidirectional long-term changes in synaptic strengths. This process includes long-term potentiation and long-term depression, which are dependent on the timing of presynaptic and postsynaptic spikings. In this review, we focus on computational aspects of signaling mechanisms that induce and maintain STDP as a key step toward the definition of a general synaptic learning rule. In addition, we discuss the temporal and spatial aspects of STDP, and the requirement of a homeostatic mechanism of STDP in vivo