Induction and propagation of transient synchronous activity in neural networks endowed with short-term plasticity

Wu, Shengdun; Zhou, Kang; Ai, Yuping; Zhou, Guanyu; Yao, Dezhong; Guo, Daqing

doi:10.1007/s11571-020-09578-6

Cited by 9 publications

(5 citation statements)

References 40 publications

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“…4H-I ). This effect is in-keeping with modelling studies that indicate enhanced propagation of synchronous neuronal firing in networks where synaptic connections are endowed with the capacity to undergo short-term facilitation 54 . Since AMPAR immobilization was also associated with fewer neurons being recruited during spontaneous network activity, this opens the possibility that AMPAR immobilization-induced changes in HF-STP could lead to deterioration of engram-to-engram cell connections and compromise reactivation of engram cells in some contexts relating to memory retrieval 55 .…”

Section: Discussionsupporting

confidence: 85%

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: Discussionsupporting

confidence: 85%

Synapse specific and plasticity-regulated AMPAR mobility tunes synaptic integration

Nowacka,

Getz,

Zieger

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…Presynaptic short-term plasticity was described by the dynamics of two variables, the amount of neurotransmitter

, and the release probability

, in Equation 3 , and was governed by a depression time constant

, and a facilitation time constant,

, as described in the following equations (

where

is the spike train of neuron

is the Dirac delta function. Depending on the firing history of a neuron, short-term depression or potentiation 31 , 78 , 79 may be induced by the depletion of neurotransmitter,

, or an increase in the release probability,

, which temporarily changes the synaptic conductance,

, in Equation 3 .…”

Section: Methodsmentioning

confidence: 99%

Memory rescue and learning in synaptic impaired neuronal circuits

Zhou

2023

iScience

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“…(3), and was governed by a depression time constant, τ D , and a facilitation time constant, τ F , as described in the following equations ( τ F » τ D ): where is the spike train of neuron i and δ ( t ) is the Dirac delta function. Depending on the firing history of a neuron, short-term depression or potentiation (Mongillo et al, 2008; Wu et al, 2020; Zucker, 2002) may be induced by the depletion of neurotransmitter, x i , or an increase in the release probability, u i , which temporarily changes the synaptic conductance, , in Eq. (3).…”

Section: Methods and Methodsmentioning

confidence: 99%

“…where ܵ ሺ‫ݐ‬ሻ ൌ ∑ ߜሺ‫ݐ‬ െ ‫ݐ‬ ሻ is the spike train of neuron ݅ and ߜሺ‫ݐ‬ሻ is the Dirac delta function. Depending on the firing history of a neuron, short-term depression or potentiation (Mongillo et al, 2008;Wu et al, 2020;Zucker, 2002) may be induced by the depletion of neurotransmitter, ‫ݔ‬ , or an increase in the release probability, ‫ݑ‬ , which temporarily changes the synaptic conductance, ‫ܩ‬ ா՜ ሺ‫ݐ‬ሻ, in Eq. ( 3).…”

Section: Short-term Plasticitymentioning

confidence: 99%

Synaptic degeneration in neuronal circuits hinders memory recall, memory rescue, and learning

Zhou

2022

Preprint

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Neurodegeneration is a characteristic of Alzheimer's disease (AD), but its effect on neural activity dynamics underlying memory deficits is unclear. Here, we studied the effects of synaptic degeneration on neural activities associated with memory recall, memory rescue by slow-gamma stimulation, and learning a new memory, in an integrate-and-fire neuronal network. Our results showed that reducing connectivity decreases the neuronal synchronisation of memory neurons at slow-gamma frequencies and impairs memory recall performance. Although slow-gamma stimulation rescued memory recall and slow-gamma oscillations, the rescue with reduced connectivity caused a side effect of activating mixed memories. During the learning of a new memory, reducing connectivity caused an impairment in storing the new memory, but did not affect previously stored memories. Our results reveal potential computational mechanisms underlying the memory deficits caused by synaptic degeneration in AD.

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Induction and propagation of transient synchronous activity in neural networks endowed with short-term plasticity

Cited by 9 publications

References 40 publications

Synapse specific and plasticity-regulated AMPAR mobility tunes synaptic integration

Synapse specific and plasticity-regulated AMPAR mobility tunes synaptic integration

Memory rescue and learning in synaptic impaired neuronal circuits

Synaptic degeneration in neuronal circuits hinders memory recall, memory rescue, and learning

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