Integrating Hebbian and homeostatic plasticity: introduction

Abstract

Hebbian plasticity is widely considered to be the mechanism by which information can be coded and retained in neurons in the brain. Homeostatic plasticity moves the neuron back towards its original state following a perturbation, including perturbations produced by Hebbian plasticity. How then does homeostatic plasticity avoid erasing the Hebbian coded information? To understand how plasticity works in the brain, and therefore to understand learning, memory, sensory adaptation, development and recovery from injury, requires development of a theory of plasticity that integrates both forms of plasticity into a whole. In April 2016, a group of computational and experimental neuroscientists met in London at a discussion meeting hosted by the Royal Society to identify the critical questions in the field and to frame the research agenda for the next steps. Here, we provide a brief introduction to the papers arising from the meeting and highlight some of the themes to have emerged from the discussions. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

Hebbian and Homeostatic Synaptic Plasticity—Do Alterations of One Reflect Enhancement of the Other?

“…Similar evidence exists for interaction between Aβ and PSD-95 (Roselli et al, 2005;Sun and Turrigiano, 2011), GKAP (Roselli et al, 2011;Shin et al, 2012), calcineurin (D'Amelio et al, 2011;Kim and Ziff, 2014) and STEP 61 (Kurup et al, 2010). Finally, BDNF and TNFα, which have been firmly linked to homeostatic synaptic plasticity Stellwagen and Malenka, 2006;Becker et al, 2015), seem to be dysregulated in the AD brain (Fillit et al, 1991;Phillips et al, 1991). Along this line of evidence, a role for microglia in Aβ-mediated alterations in complex brain function has been suggested (Kitazawa et al, 2004;Hansen et al, 2018;Kinney et al, 2018;Hemonnot et al, 2019).…”

Disruption of NMDAR Function Prevents Normal Experience-Dependent Homeostatic Synaptic Plasticity in Mouse Primary Visual Cortex

“…The mechanisms of homeostatic adaptation to changes in sensory experience has been largely explained by two distinct models: sliding threshold and synaptic scaling. Although these two models are considered different, there is emerging body of recent work suggesting that these two modes of homeostatic plasticity may share similarities and may interact with each other to regulate synaptic strength (for recent discussions, see Fox and Stryker, 2017;Keck et al, 2017). Furthermore, there is evidence that sliding threshold or synaptic scaling mode of homeostatic plasticity may be used depending on the regime of activity changes in vivo (Bridi et al, 2018).…”

Assessing the kaleidoscope of monocular deprivation effects

“…Taken together, it seemed that feedforward, contrast energy-based models of deprivation sufficed to explain these effects. Under this idea, deprivation triggers interocular contrast gain control (Moradi & Heeger, 2009;Shapley & Enroth-Cugell, 1984;Sperling & Ding, 2010), whereby gain is increased in the deprived eye and decreased in the nondeprived eye (Zhou, Clavagnier, et al, 2013) in an assumedly compensatory, homeostatic attempt (Fox & Stryker, 2017;Turrigiano & Nelson, 2000) to restore interocular balance. Upon resumption of normal binocular vision, observed deprivation effects, then, reflect the persistence of this reweighting, giving the deprived eye greater inhibitory influence over the contralateral eye and thereby greater representation in binocular/dichoptic tasks and percepts, for up to 30 min (Zhou, Clavagnier, et al, 2013).…”