Short-term plasticity as a mechanism to regulate and retain multistability

Zhou, Xinjia; Tian, Changhai; Zhang, Xiyun; Zheng, Muhua; Xu, Kesheng

doi:10.1016/j.chaos.2022.112891

Cited by 5 publications

(1 citation statement)

References 53 publications

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“…The observed network effect associated with reduced summation of synaptic responses at high-frequencies is consistent with a putative role of synaptic depression in gain control - to dampen the strength of synapses during ongoing, repetitive pre-synaptic activity. The extent of gain control observed could also have been enhanced by the selective enhancement of short term-depression only at excitatory inputs, effectively acting then to reduce excitatory/inhibitory balance and dampen neuronal network activity as firing frequency increases 53 . Another effect on spontaneous neuronal network observed after AMPAR immobilization-induced depression of burst responses was a lower coherence of neuronal firing, as measured by reduction in the pairwise correlation of neuronal firing across the network of neurons in hippocampal slice cultures ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Synapse specific and plasticity-regulated AMPAR mobility tunes synaptic integration

Nowacka,

Getz,

Zieger

et al. 2024

Preprint

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Synaptic responses adapt to fast repetitive inputs during bursts of neuronal network activity over timescales of milliseconds to seconds, either transiently facilitating or depressing. This high-frequency stimulus-dependent short-term synaptic plasticity (HF-STP) relies on a number of molecular processes that collectively endow synapses with filtering properties for information processing, optimized for the transmission of certain input frequencies and patterns in distinct circuits1–3. Changes in HF-STP are traditionally thought to stem from changes in pre-synaptic transmitter release1,2, but post-synaptic modifications in receptor biophysical properties or surface diffusion also regulate HF-STP4–11. A major challenge in understanding synapse function is to decipher how pre- and post-synaptic mechanisms synergistically tune synaptic transmission efficacy during HF-STP, and to determine how neuronal activity modifies post-synaptic signal computation and integration to diversify neuronal circuit function. Here, taking advantage of new molecular tools to directly visualize glutamate release12and specifically manipulate the surface diffusion of endogenous AMPAR in intact circuits13, we define the respective contributions of pre-synaptic glutamate release, AMPAR desensitization and surface mobility to frequency-dependent synaptic adaptation. We demonstrate that post-synaptic gain control and signal integration capacity in synaptic networks is influenced by synapse-specific differences in AMPAR desensitization and diffusion-trapping characteristics that are shaped by molecular signaling events recruited during LTP.

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Section: Discussionmentioning

confidence: 99%