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Synaptic Time-Dependent Plasticity Leads to Efficient Coding of Predictions

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 Publication date 2019
  fields Biology
and research's language is English




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Latency reduction of postsynaptic spikes is a well-known effect of Synaptic Time-Dependent Plasticity. We expand this notion for long postsynaptic spike trains, showing that, for a fixed input spike train, STDP reduces the number of postsynaptic spikes and concentrates the remaining ones. Then we study the consequences of this phenomena in terms of coding, finding that this mechanism improves the neural code by increasing the signal-to-noise ratio and lowering the metabolic costs of frequent stimuli. Finally, we illustrate that the reduction of postsynaptic latencies can lead to the emergence of predictions.



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We show that the local Spike Timing-Dependent Plasticity (STDP) rule has the effect of regulating the trans-synaptic weights of loops of any length within a simulated network of neurons. We show that depending on STDPs polarity, functional loops are formed or eliminated in networks driven to normal spiking conditions by random, partially correlated inputs, where functional loops comprise weights that exceed a non-zero threshold. We further prove that STDP is a form of loop-regulating plasticity for the case of a linear network comprising random weights drawn from certain distributions. Thus a notable local synaptic learning rule makes a specific prediction about synapses in the brain in which standard STDP is present: that under normal spiking conditions, they should participate in predominantly feed-forward connections at all scales. Our model implies that any deviations from this prediction would require a substantial modification to the hypothesized role for standard STDP. Given its widespread occurrence in the brain, we predict that STDP could also regulate long range synaptic loops among individual neurons across all brain scales, up to, and including, the scale of global brain network topology.
Synaptic plasticity is the capacity of a preexisting connection between two neurons to change in strength as a function of neural activity. Because synaptic plasticity is the major candidate mechanism for learning and memory, the elucidation of its constituting mechanisms is of crucial importance in many aspects of normal and pathological brain function. In particular, a prominent aspect that remains debated is how the plasticity mechanisms, that encompass a broad spectrum of temporal and spatial scales, come to play together in a concerted fashion. Here we review and discuss evidence that pinpoints to a possible non-neuronal, glial candidate for such orchestration: the regulation of synaptic plasticity by astrocytes.
Brain plasticity refers to brains ability to change neuronal connections, as a result of environmental stimuli, new experiences, or damage. In this work, we study the effects of the synaptic delay on both the coupling strengths and synchronisation in a neuronal network with synaptic plasticity. We build a network of Hodgkin-Huxley neurons, where the plasticity is given by the Hebbian rules. We verify that without time delay the excitatory synapses became stronger from the high frequency to low frequency neurons and the inhibitory synapses increases in the opposite way, when the delay is increased the network presents a non-trivial topology. Regarding the synchronisation, only for small values of the synaptic delay this phenomenon is observed.
Neural populations exposed to a certain stimulus learn to represent it better. However, the process that leads local, self-organized rules to do so is unclear. We address the question of how can a neural periodic input be learned and use the Differential Hebbian Learning framework, coupled with a homeostatic mechanism to derive two self-consistency equations that lead to increased responses to the same stimulus. Although all our simulations are done with simple Leaky-Integrate and Fire neurons and standard Spiking Time Dependent Plasticity learning rules, our results can be easily interpreted in terms of rates and population codes.
Coarse-graining microscopic models of biological neural networks to obtain mesoscopic models of neural activities is an essential step towards multi-scale models of the brain. Here, we extend a recent theory for mesoscopic population dynamics with static synapses to the case of dynamic synapses exhibiting short-term plasticity (STP). Under the assumption that spike arrivals at synapses have Poisson statistics, we derive analytically stochastic mean-field dynamics for the effective synaptic coupling between finite-size populations undergoing Tsodyks-Markram STP. The novel mean-field equations account for both finite number of synapses and correlations between the neurotransmitter release probability and the fraction of available synaptic resources. Comparisons with Monte Carlo simulations of the microscopic model show that in both feedforward and recurrent networks the mesoscopic mean-field model accurately reproduces stochastic realizations of the total synaptic input into a postsynaptic neuron and accounts for stochastic switches between Up and Down states as well as for population spikes. The extended mesoscopic population theory of spiking neural networks with STP may be useful for a systematic reduction of detailed biophysical models of cortical microcircuits to efficient and mathematically tractable mean-field models.
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