bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.09.04.749460

Plateau-gated one-shot plasticity supports continual recognition memory

Abstract

Biological memory systems store single experiences while continuing to learn, but how one-shot plasticity limits interference with existing memories is unclear. Behavioral timescale synaptic plasticity (BTSP) rapidly modifies synapses active within seconds of a dendritic plateau. We isolate its plateau-triggered component in a model where plastic weights and a stable instructive pathway jointly determine whether a plateau occurs, closing a feedback loop between the synaptic state and the plastic event that modifies it. For unstructured inputs, instantiated by independent uniform signed patterns, the dynamics reduce exactly to pathway alignment, which determines the fidelity of the instructed representation, the synaptic-turnover rate and the mean rewrite interval. For structured inputs, instantiated by correlated bimodal Curie--Weiss patterns, the instructive pathway biases which component of input structure enters the plastic synaptic state. In a BTSP-inspired continual-recognition network, combined instructive and plastic drives determined the selected memory unit for each one-shot write, whereas a Hebbian control used the same plastic weights for credit assignment and memory storage. The BTSP-inspired network remained accurate at longer repeat lags than Hebbian controls, an advantage that grew with network size, with both architectures optimized independently at every repeat lag. A reduced theory predicted held-out accuracy, lag capacity and dynamics of memory-trace strength directly from optimized parameters. It showed why intermediate proximal and distal coupling was optimal: proximal plastic drive guided plateau generation toward selected memory units, slowing synaptic turnover but limiting new encoding, whereas distal instructive drive enhanced familiar responses but could also make novel inputs appear familiar. The memory-trace strength in the rate-and-depth-matched Hebbian control still decayed faster and showed less effective credit assignment than in the BTSP-inspired network. These results connect dendritic plateau physiology to continual memory and support partial separation of allocation from storage as a mechanism for limiting interference during continual learning.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Li, G., Romani, S., Magee, J. C.. 2026-09-11. Plateau-gated one-shot plasticity supports continual recognition memory. https://doi.org/10.64898/2026.09.04.749460

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

A systems-level model of sleep-dependent memory-consolidation failure in neurodegeneration: the spindle-slow-oscillation decoupling cascade dissociates amyloid and tau

During non-rapid-eye-movement (NREM) sleep, the temporal coupling of cortical slow oscillations (SOs), thalamic spindles, and hippocampal sharp wave ripples drives the consolidation of declarative memories. This coupling degrades in ageing and Alzheimers disease (AD), and although A{beta} and tau leave dissociable signatures in human sleep, the mechanisms by which progressive pathology dismantles the consolidation machinery are difficult to isolate experimentally, and have not to our knowledge been reproduced in a model that can be perturbed directly. We built a systems-level model in which cortical SOs and thalamic spindles are generated by reduced oscillators, hippocampal ripples replay encoded spike sequences, and the measured per-event SO-spindle timing alignment causally gates spike-timing dependent plasticity on cortical sequence synapses. A post-sleep cued-recall test reads out consolidation. Five neurodegeneration parameters (amyloid, tau, synaptic density, GABAergic inhibition, cholinergic tone) map to dis tinct mechanisms grounded in the human and animal literature. The model reproduces graded healthy consolidation and a progressive collapse in which coupling, slow-wave power, spindle power and recall fall monotonically and the overnight memory effect flips from consolidation to net forgetting, with weak memories failing first. Scrambling SO-spindle timing while holding oscillation power fixed abolishes consolidation, establishing that coupling timing, rather than oscillation power, is what the plasticity gate depends on within the model. A{beta} and tau impair memory through orthogonal signatures (A{beta} collapses slow-wave power while sparing replay order, tau the reverse) and this orthogonality holds across the entire A{beta} x tau plane and survives simultaneous {+/-}50% resampling of every mapping coefficient (40/40 samples), so it is not an artefact of a single calibration point. The model yields a falsifiable clinical prediction: closed-loop slow-oscillation enhancement rescues memory only when the deficit is amplitude/coupling-dominated, not when it is replay(tau)-dominated, despite normalising slow-wave power in both cases. Because the therapy arms dissociate coupling from memory benefit, the model also cautions against adopting SO-spindle coupling as a standalone surrogate endpoint.

neuroscience↗

Toxicity of MAPT 4R RNA Contributes to Motor Neuron Degeneration in ALS

MAPT (Tau) dysregulation is implicated in several neurodegenerative diseases, but its contribution to amyotrophic lateral sclerosis (ALS) is poorly understood. Here we show that mRNA isoforms encoding 4-repeat (4R) Tau are upregulated and cytoplasmically enriched in iPSC-derived motor neurons (MNs) from VCP-mutant and sporadic ALS, without a corresponding change in Tau protein. Using splice-switching antisense oligonucleotides and isoform-specific siRNAs, we find that enhanced 4R expression reduces MN viability, whereas its selective knockdown improves survival, with kinetics more consistent with an RNA-intrinsic effect than altered protein synthesis. Exon 10-containing MAPT RNA shows increased predicted secondary structure, self-association and altered Tau biocondensation in vitro. In post-mortem ALS cervical spinal cord, increased relative exon 10 usage is associated with a higher-risk clinical phenotype and shorter disease duration These findings identify an isoform-specific contribution of MAPT to MN vulnerability in ALS and nominate 4R MAPT RNA as a therapeutic target.

neuroscience↗

State dependant modulation of optic flow-processing lobula plate cells in butterflies

Increasing experimental evidence suggests that biological systems cancel predictable components of sensory signals while maintaining sensitivity to externally induced state changes. This strategy provides task-specific sensor responses for posture, locomotion, and gaze control. A prime example is found in interneurons that respond to visual image shifts resulting from the relative motion between an animal's eyes and its visual surroundings. Such optic flow-processing interneurons, found across phyla and are particularly well characterized in Dipteran and other flying insects. We studied optic flow-processing interneurons in the Monarch butterfly whose large and highly contrasted wings sweep through the visual field with every wing-beat cycle, potentially obscuring interneuron output signals. Our results show baseline spiking activity increases when animals flap their wings, and individual spikes are phase-locked to the wing-beat cycle, even in the dark, when no visual motion input is available. A qualitative estimate of the interneurons' response to directional wing motion through its receptive field is not sufficient to explain the recorded activity patterns. Our results suggest that an additional internal signal suppresses responses to wing-induced visual motion to support effective vision-based stabilization reflexes. These findings support the principle that self-generated signals are suppressed while sensitivity to external modulation is preserved.

neuroscience↗