Integrating Hebbian and homeostatic plasticity: the current state of the field and future research directions

Keck, Tara; Toyoizumi, Taro; Chen, Lu; Doiron, Brent; Feldman, Daniel E.; Fox, Kevin; Gerstner, Wulfram; Haydon, Philip G.; Hübener, Mark; Lee, Hey Kyoung; Lisman, John; Rose, Tobias; Sengpiel, Frank; Stellwagen, David; Stryker, Michael P.; Turrigiano, Gina G.; Rossum, Mark C. W. van

doi:10.1098/rstb.2016.0158

Cited by 176 publications

(192 citation statements)

References 106 publications

(225 reference statements)

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“…Keck et al [16] point out that activity-independent spine fluctuations could temper the runaway increase in synaptic strength that can result from Hebbian mechanisms. Spine sizes are known to fluctuate in vivo independently of activity, and the fluctuations are proportional to the size of the synapse.…”

Section: A Question Of Scalementioning

confidence: 99%

“…Is homeostasis maintained at the level of the individual synapse, the individual dendrite, the whole neuron, the circuit level, or at all of the above? Toyoizumi and co-workers have concluded that stability of neuronal responses can be attained if slow homeostatic and fast Hebbian plasticity operate at different sites [16,21]. At the macroscopic end of this scale, one might imagine that glial cells are ideally placed to coordinate homeostatic plasticity over a wide area of the brain.…”

Section: A Question Of Scalementioning

confidence: 99%

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Integrating Hebbian and homeostatic plasticity: introduction

Fox

Stryker

2017

Phil. Trans. R. Soc. B

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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’.

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Section: A Question Of Scalementioning

confidence: 99%

Section: A Question Of Scalementioning

confidence: 99%

Integrating Hebbian and homeostatic plasticity: introduction

Fox

Stryker

2017

Phil. Trans. R. Soc. B

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“…Homeostatic and Hebbian plasticity work in coherence to establish cortical maps, but their mechanisms differ significantly (Feldman and Brecht, 2005;Gainey and Feldman, 2017;Keck et al, 2017). Alternative deprivation or stimulation methods, such as single-row whisker deprivation or single-whisker experience (Allen et al, 2003;Celikel et al, 2004;Clem et al, 2008;Foeller et al, 2005), result in electrophysiologically well-defined plasticity phenotypes, the molecular mechanisms of which have been poorly studied and still require elucidation.…”

Section: ) From Synaptic Plasticity To Synaptic Disordersmentioning

confidence: 99%

Cellular diversity of the somatosensory cortical map plasticity

Kole

Scheenen

Tiesinga

et al. 2018

Neuroscience & Biobehavioral Reviews

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Sensory maps are representations of the sensory epithelia in the brain. Despite the intuitive explanatory power behind sensory maps as being neuronal precursors to sensory perception, and sensory cortical plasticity as a neural correlate of perceptual learning, molecular mechanisms that regulate map plasticity are not well understood. Here we perform a meta-analysis of transcriptional and translational changes during altered whisker use to nominate the major molecular correlates of experience-dependent map plasticity in the barrel cortex. We argue that brain plasticity is a systems level response, involving all cell classes, from neuron and glia to non-neuronal cells including endothelia. Using molecular pathway analysis, we further propose a gene regulatory network that could couple activity dependent changes in neurons to adaptive changes in neurovasculature, and finally we show that transcriptional regulations observed in major brain disorders target genes that are modulated by altered sensory experience. Thus, understanding the molecular mechanisms of experience-dependent plasticity of sensory maps might help to unravel the cellular events that shape brain plasticity in health and disease. peer-reviewed)

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“…HSP and Hebbian plasticity are theoretically both required for normal circuit function: HSP is designed to maintain circuit function, whereas Hebbian plasticity is designed to change circuit function, so that the same input will now lead to a different output/behaviour (a minimalistic framing of learning). These processes must be balanced-pure HSP would prevent any learning, while if Hebbian processes dominate, then the network becomes very unstable [21,22]. Given the specificity of TNF to HSP and not Hebbian plasticity [16,23], this is a potential route to probe the role of HSP in neurodevelopment and behaviour.…”

Section: Introductionmentioning

confidence: 99%

Tumour necrosis factor-mediated homeostatic synaptic plasticity in behavioural models: testing a role in maternal immune activation

Konefal

Stellwagen

2017

Phil. Trans. R. Soc. B

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The proinflammatory cytokine tumour necrosis factor-alpha (TNFa) has long been characterized for its role in the innate immune system, but more recently has been found to have a distinct role in the nervous system that does not overlap with other proinflammatory cytokines. Through regulation of neuronal glutamate and GABA receptor trafficking, TNF mediates a homeostatic form of synaptic plasticity, but plays no direct role in Hebbian forms of plasticity. As yet, there is no evidence to suggest that this adaptive plasticity plays a significant role in normal development, but it does maintain neuronal circuit function in the face of several types of disruption. This includes developmental plasticity in primary sensory cortices, as well as modulating the response to antidepressants, chronic antipsychotics and drugs of abuse. TNF is also a prominent component of the neuroinflammation occurring in most neuropathologies, but the role of TNF-mediated synaptic plasticity in this context remains to be determined. We tested this in a maternal immune activation (MIA) model of neurodevelopmental disorders. Using TNF 2/2 mice, we observed that TNF is not required for the expression of abnormal social or anxious behaviour in this model. This indicates that TNF does not uniquely contribute to the development of neuronal dysfunction in this model, and suggests that during neuroinflammatory events, compensation between the various proinflammatory cytokines is the norm. This article is part of the themed issue 'Integrating Hebbian and homeostatic plasticity'.

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Integrating Hebbian and homeostatic plasticity: the current state of the field and future research directions

Cited by 176 publications

References 106 publications

Integrating Hebbian and homeostatic plasticity: introduction

Integrating Hebbian and homeostatic plasticity: introduction

Cellular diversity of the somatosensory cortical map plasticity

Tumour necrosis factor-mediated homeostatic synaptic plasticity in behavioural models: testing a role in maternal immune activation

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