Spike-timing-dependent plasticity rewards synchrony rather than causality

Abstract

Spike-timing-dependent plasticity (STDP) is a candidate mechanism for information storage in the brain. However, it has been practically impossible to assess the long-term consequences of STDP as recordings from postsynaptic neurons last at most one hour. We assessed both the short-term (20 minutes) and long-term (3 days) effects of optically-induced STDP (oSTDP) using two colors of light to independently activate CA3 and CA1 neurons expressing the opsins ChrimsonR and CheRiff. During patch-clamp recordings short-term effects followed classic STDP rules, synapses potentiated when postsynaptic spikes followed presynaptic spikes (tLTP, causal pairing) and depressed when postsynaptic spikes were first (tLTD, anti-causal pairing). Surprisingly, three days after inducing oSTDP without patching the neurons, tLTP was evident regardless of pairing sequence. Potentiation depended on NMDA receptors and spontaneous activity was necessary in the two days following oSTDP. Our data suggest that tLTD at Schaffer collateral synapses is a transitory phenomenon or a recording artifact.

Predictive coding of natural images by V1 firing rates and rhythmic synchronization

“…It is known that synchronization can have important consequences for the induction of synaptic plasticity ( Galuske et al., 2019 ; Sejnowski and Paulsen, 2006 ; Stopfer et al., 1997 ), which is mediated by mechanisms such as spike-timing-dependent plasticity ( Wespatat et al., 2004 ; Sjöström et al., 2001 ; Sejnowski and Paulsen, 2006 ; Vinck et al., 2010 ; Galuske et al., 2019 ; Anisimova et al., 2021 ). Bursts of γ oscillations could therefore maintain or strengthen synaptic connections between neurons that, on average, predict each other’s visual inputs, and thereby contribute to self-supervised learning of spatiotemporal natural image statistics.…”

<em>Ex Vivo</em> Optogenetic Interrogation of Long-Range Synaptic Transmission and Plasticity from Medial Prefrontal Cortex to Lateral Entorhinal Cortex

“…ChrimsonR retains low-sensitivity to blue light, thus to avoid cross pathway activation it can be used in combination with red-insensitive opsins, which are violet shifted (CheRiff 27 ) and/or have orders of magnitude higher sensitivity to blue light (Chronos 26 ). This allows for the use of blue/violet light stimuli which are too weak to significantly activate ChrimsonR and therefore allow activation of two pathways 39,40 , which may increase experimental throughput, allow examination of convergent pathway interactions, and allow the release of neuromodulators from endogenous sources 41 .…”