Recent results have demonstrated modification of electrical synapse strength by varied forms of neuronal activity. However, the mechanisms underlying plasticity induction in central mammalian neurons are unclear. Here we show that the two established inductors of plasticity at electrical synapses in the thalamic reticular nucleus -- paired burst spiking in coupled neurons, and mGluR-dependent tetanization of synaptic input -- are separate pathways that converge at a common downstream endpoint. Using occlusion experiments and pharmacology in patched pairs of coupled neurons in vitro, we show that burst-induced depression depends on calcium entry via voltage-gated channels, is blocked by BAPTA chelation, and recruits intracellular calcium release on its way to activation of phosphatase activity. In contrast, mGluR-dependent plasticity is independent of calcium entry or calcium dynamics. Together, these results show that the spiking-initiated mechanisms underlying electrical synapse plasticity are similar to those that induce plasticity at chemical synapses, and offer the possibility that calcium-regulated mechanisms may also lead to alternate outcomes, such as potentiation. Because these mechanistic elements are widely found in mature neurons, we expect them to apply broadly to electrical synapses across the brain, acting as the crucial link between neuronal activity and electrical synapse strength.
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A calcium-dependent pathway underlies activity-dependent plasticity of electrical synapses in the thalamic reticular nucleus: Calcium and plasticity of electrical synapses
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3D sensing is a primitive function that allows imaging with depth information generally achieved via the time‐of‐flight (ToF) principle. However, time‐to‐digital converters (TDCs) in conventional ToF sensors are usually bulky, complex, and exhibit large delay and power loss. To overcome these issues, a resistive time‐of‐flight (R‐ToF) sensor that can measure the depth information in an analog domain by mimicking the biological process of spike‐timing‐dependent plasticity (STDP) is proposed herein. The R‐ToF sensors based on integrated avalanche photodiodes (APDs) with memristive intelligent matters achieve a scan depth of up to 55 cm (≈89% accuracy and 2.93 cm standard deviation) and low power consumption (0.5 nJ/step) without TDCs. The in‐depth computing is realized via R‐ToF 3D imaging and memristive classification. This R‐ToF system opens a new pathway for miniaturized and energy‐efficient neuromorphic vision engineering that can be harnessed in light‐detection and ranging (LiDAR), automotive vehicles, biomedical in vivo imaging, and augmented/virtual reality.
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The Liquid State Machine (LSM) is a promising model of recurrent spiking neural networks. It consists of a fixed recurrent network, or the reservoir, which projects to a readout layer through plastic readout synapses. The classification performance is highly dependent on the training of readout synapses which tend to be very dense and contribute significantly to the overall network complexity. We present a unifying biologically inspired calcium-modulated supervised spike-timing dependent plasticity (STDP) approach to training and sparsification of readout synapses, where supervised temporal learning is modulated by the post-synaptic firing level characterized by the post-synaptic calcium concentration. The proposed approach prevents synaptic weight saturation, boosts learning performance, and sparsifies the connectivity between the reservoir and readout layer. Using the recognition rate of spoken English letters adopted from the TI46 speech corpus as a measure of performance, we demonstrate that the proposed approach outperforms a baseline supervised STDP mechanism by up to 25%, and a competitive non-STDP spike-dependent training algorithm by up to 2.7%. Furthermore, it can prune out up to 30% of readout synapses without causing significant performance degradation.more » « less
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Abstract The
Drosophila mushroom body (MB) is an important model system for studying the synaptic mechanisms of associative learning. In this system, coincidence of odor-evoked calcium influx and dopaminergic input in the presynaptic terminals of Kenyon cells (KCs), the principal neurons of the MB, triggers long-term depression (LTD), which plays a critical role in olfactory learning. However, it is controversial whether such synaptic plasticity is accompanied by a corresponding decrease in odor-evoked calcium activity in the KC presynaptic terminals. Here, we address this question by inducing LTD by pairing odor presentation with optogenetic activation of dopaminergic neurons (DANs). This allows us to rigorously compare the changes at the presynaptic and postsynaptic sites in the same conditions. By imaging presynaptic acetylcholine release in the condition where LTD is reliably observed in the postsynaptic calcium signals, we show that neurotransmitter release from KCs is depressed selectively in the MB compartments innervated by activated DANs, demonstrating the presynaptic nature of LTD. However, total odor-evoked calcium activity of the KC axon bundles does not show concurrent depression. We further conduct calcium imaging in individual presynaptic boutons and uncover the highly heterogeneous nature of calcium plasticity. Namely, only a subset of boutons, which are strongly activated by associated odors, undergo calcium activity depression, while weakly responding boutons show potentiation. Thus, our results suggest an unexpected nonlinear relationship between presynaptic calcium influx and the results of plasticity, challenging the simple view of cooperative actions of presynaptic calcium and dopaminergic input.
