A Voltage-Based STDP Rule Combined with Fast BCM-Like Metaplasticity Accounts for LTP and Concurrent “Heterosynaptic” LTD in the Dentate Gyrus In Vivo

Jedlicka, Paul; Benuskova, Lubica; Abraham, Wickliffe C.

doi:10.1371/journal.pcbi.1004588

Cited by 46 publications

(70 citation statements)

References 52 publications

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“…[23] corroborates the above findings. By fitting their model with a rapid sliding threshold to in vivo data from dentate gyrus, the authors find τ y ≈ 12 s which allows them to speculate that the sliding threshold could be linked to CaMKII inactivation.…”

Section: How Fast Do Compensatory Processes Have To Be?supporting

confidence: 84%

“…First, heterosynaptic plasticity not only stabilizes Hebbian plasticity in the active pathway, it also introduces synaptic competition between the active and the control pathway (figure 5 g ). In contrast to BCM-like models in which heterosynaptic depression of the inactive pathway depends on intermediate periods of background activity in between stimuli [23,88], here the heterosynaptic depression happens simultaneously with LTP induction (figure 5 g ). Second, although the learning rule effectively implements a rapid redistribution of synaptic weights reminiscent of synaptic scaling, it is still a fully local learning rule which only depends on information that is available at the synapse (cf.…”

Section: Learning and Recall In A Recurrent Spiking Network Modelmentioning

confidence: 77%

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Hebbian plasticity requires compensatory processes on multiple timescales

Zenke

Gerstner

2017

Phil. Trans. R. Soc. B

179

209

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We review a body of theoretical and experimental research on Hebbian and homeostatic plasticity, starting from a puzzling observation: while homeostasis of synapses found in experiments is a slow compensatory process, most mathematical models of synaptic plasticity use rapid compensatory processes (RCPs). Even worse, with the slow homeostatic plasticity reported in experiments, simulations of existing plasticity models cannot maintain network stability unless further control mechanisms are implemented. To solve this paradox, we suggest that in addition to slow forms of homeostatic plasticity there are RCPs which stabilize synaptic plasticity on short timescales. These rapid processes may include heterosynaptic depression triggered by episodes of high postsynaptic firing rate. While slower forms of homeostatic plasticity are not sufficient to stabilize Hebbian plasticity, they are important for fine-tuning neural circuits. Taken together we suggest that learning and memory rely on an intricate interplay of diverse plasticity mechanisms on different timescales which jointly ensure stability and plasticity of neural circuits.This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

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Section: How Fast Do Compensatory Processes Have To Be?supporting

confidence: 84%

Section: Learning and Recall In A Recurrent Spiking Network Modelmentioning

confidence: 77%

Hebbian plasticity requires compensatory processes on multiple timescales

Zenke

Gerstner

2017

Phil. Trans. R. Soc. B

179

209

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“…However, there are several lines of theoretical and experimental evidence, spanning several synaptic and intrinsic components as candidate mechanisms, for concurrent emergence of encoding, stability and activity homeostasis. These lines of evidence also argue for prominent advantages when encoding, homeostasis and stability mechanisms are concurrent (Abraham, Logan, Wolff, & Benuskova, ; Anirudhan & Narayanan, ; Benuskova & Abraham, ; Honnuraiah & Narayanan, ; Ibata, Sun, & Turrigiano, ; Jedlicka et al, ; Johnston & Narayanan, ; Narayanan & Johnston, ; Narayanan & Johnston, ; Nelson & Turrigiano, ; O'Leary et al, ; Triesch, ; Turrigiano, ; Turrigiano, ; Turrigiano, ; Zenke et al, ).…”

Section: Degeneracy At Multiple Scales In the Hippocampusmentioning

confidence: 99%

“…In the absence of concomitant homeostatic mechanisms, Hebbian plasticity would result in runaway excitation (Figure ). Several theories and mechanisms have been proposed as a means to avoid this runaway excitation (Abbott, ; Abraham & Robins, ; Benuskova & Abraham, ; Honnuraiah & Narayanan, ; Jedlicka, Benuskova, & Abraham, ; Korte & Schmitz, ; Miller & MacKay, ; Nelson & Turrigiano, ; Turrigiano, ; Turrigiano, ; Turrigiano, ; Turrigiano, ; Turrigiano, ; Turrigiano & Nelson, ; van Rossum, Bi, & Turrigiano, ; Zenke, Gerstner, & Ganguli, ). A prominent theme that spans several such stability theories is metaplasticity (Abraham, ; Abraham & Bear, ; Abraham & Tate, ; Hulme et al, ), where the profile of plasticity concomitantly changes with the induction of plasticity (Figure a,b).…”

Section: Degeneracy At Multiple Scales In the Hippocampusmentioning

confidence: 99%

Degeneracy in hippocampal physiology and plasticity

2019

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Degeneracy, defined as the ability of structurally disparate elements to perform analogous function, has largely been assessed from the perspective of maintaining robustness of physiology or plasticity. How does the framework of degeneracy assimilate into an encoding system where the ability to change is an essential ingredient for storing new incoming information? Could degeneracy maintain the balance between the apparently contradictory goals of the need to change for encoding and the need to resist change towards maintaining homeostasis? In this review, we explore these fundamental questions with the mammalian hippocampus as an example encoding system. We systematically catalog lines of evidence, spanning multiple scales of analysis that point to the expression of degeneracy in hippocampal physiology and plasticity. We assess the potential of degeneracy as a framework to achieve the conjoint goals of encoding and homeostasis without cross‐interferences. We postulate that biological complexity, involving interactions among the numerous parameters spanning different scales of analysis, could establish disparate routes towards accomplishing these conjoint goals. These disparate routes then provide several degrees of freedom to the encoding‐homeostasis system in accomplishing its tasks in an input‐ and state‐dependent manner. Finally, the expression of degeneracy spanning multiple scales offers an ideal reconciliation to several outstanding controversies, through the recognition that the seemingly contradictory disparate observations are merely alternate routes that the system might recruit towards accomplishment of its goals.

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“…(1) and which can be much faster, ∼ minutes [70,71].) On the other hand, the time constant τ θ must be smaller than about 3 min for stability reasons [47,77], and it even has been estimated as small as ∼ 12 sec [78]. Consequently, for times of the order of τ w , we have dθ/dt ≈ 0, which implies that θ ≈ αr 2 .…”

Section: Resultsmentioning

confidence: 97%

Energetics of stochastic BCM type synaptic plasticity and storing of accurate information

Karbowski

2020

Preprint

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Excitatory synaptic signaling in cortical circuits is thought to be metabolically expensive. Two fundamental brain functions, learning and memory, are associated with long-term synaptic plasticity, but we know very little about energetics of these slow biophysical processes. This study investigates the interplay between stochastic BCM type synaptic plasticity, its metabolic requirements, and the accuracy and retention of stored information in synaptic weights, within the frameworks of stochastic dynamical systems and nonequilibrium thermodynamics. The dynamic mean-field is derived for the synaptic weights, and it is found that the energy used by plastic synapses, related to their information content, is primarily caused by fluctuations in the synaptic weights and in presynaptic firing activity. Such information-related plasticity energy rate, together with the accuracy of stored information depend nonlinearly on key neurophysiological parameters, which is due to bistability in the system: synapses plus their postsynaptic neuron. At the onset of bistability, the memory lifetime, its accuracy, and plasticity energy rate are all positively correlated and exhibit sharp peaks. However, in the bistable regime, the accuracy of encoded information and plasticity energetics are generally anticorrelated, which suggests that a precise storing of synaptic information neither has to be metabolically expensive nor it is limited by energy consumption. Interestingly, such a limit on synaptic coding accuracy is imposed instead by a derivative of the plasticity energy rate with respect to the presynaptic firing, and this relationship has Keywords: energy cost of synaptic plasticity; accurate storing of synaptic information; bistability; memory lifetime; metabolism; thermodynamic limits on memory.

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A Voltage-Based STDP Rule Combined with Fast BCM-Like Metaplasticity Accounts for LTP and Concurrent “Heterosynaptic” LTD in the Dentate Gyrus In Vivo

Cited by 46 publications

References 52 publications

Hebbian plasticity requires compensatory processes on multiple timescales

Hebbian plasticity requires compensatory processes on multiple timescales

Degeneracy in hippocampal physiology and plasticity

Energetics of stochastic BCM type synaptic plasticity and storing of accurate information

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