Homeostatic plasticity induced by brief activity deprivation enhances long-term potentiation in the mature rat hippocampus

Félix-Oliveira, Afonso; Dias, Raquel B.; Colino-Oliveira, Mariana; Rombo, Diogo M.; Sebastião, Ana M.

doi:10.1152/jn.00058.2014

Cited by 22 publications

(19 citation statements)

References 58 publications

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“…For example, it has been shown in mice that retinal silencing with TTX can promote bursting in the LGN (41) and burst stimulation of the geniculate can potentiate VEPs (59). Homeostatic adaptations that facilitate experience-dependent synaptic potentiation (24,60,61), such as reduced cortical inhibition and alterations in the properties of NMDA receptors (62-64), could also contribute to the therapeutic effects of retinal inactivation. We are encouraged to believe that the approach described here, and/or the knowledge gained by studying it, might ultimately have therapeutic potential for the treatment of amblyopia and other types of neurological rehabilitation.…”

Section: Discussionmentioning

confidence: 99%

Rapid recovery from the effects of early monocular deprivation is enabled by temporary inactivation of the retinas

Fong

Mitchell

Duffy

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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A half-century of research on the consequences of monocular deprivation (MD) in animals has revealed a great deal about the pathophysiology of amblyopia. MD initiates synaptic changes in the visual cortex that reduce acuity and binocular vision by causing neurons to lose responsiveness to the deprived eye. However, much less is known about how deprivation-induced synaptic modifications can be reversed to restore normal visual function. One theoretically motivated hypothesis is that a period of inactivity can reduce the threshold for synaptic potentiation such that subsequent visual experience promotes synaptic strengthening and increased responsiveness in the visual cortex. Here we have reduced this idea to practice in two species. In young mice, we show that the otherwise stable loss of cortical responsiveness caused by MD is reversed when binocular visual experience follows temporary anesthetic inactivation of the retinas. In 3-mo-old kittens, we show that a severe impairment of visual acuity is also fully reversed by binocular experience following treatment and, further, that prolonged retinal inactivation alone can erase anatomical consequences of MD. We conclude that temporary retinal inactivation represents a highly efficacious means to promote recovery of function. A mblyopia is a widespread form of human visual disability that arises from imbalanced visual experience in the two eyes during infancy or early childhood. The core pathophysiological process underlying amblyopia is ocular dominance plasticity in the primary visual cortex (V1). Ocular dominance plasticity, evolutionarily conserved in mammals with binocular vision, has become a classic paradigm for studying how brain development is influenced by experience and deprivation. A brief period of monocular deprivation (MD) during early postnatal life causes functional depression of synapses in V1 that serve the deprived eye (1-7). Consequently, early-life MD severely and persistently degrades visual acuity through the deprived eye, which typically fails to recover spontaneously when binocular vision is restored (8-10). A critical step in developing targeted interventions for treating amblyopia is to identify strategies for reversing deprivation-driven synaptic modifications in V1.The traditional approach to promote recovery following MD has been to occlude the strong eye to force vision through the weak amblyopic eye. This "reverse occlusion" approach has been validated in animals (11, 12) and represents the cornerstone of current treatment (patching therapy) of human amblyopia (13-16). However, this treatment has well-known limitations that include poor compliance, potential loss of vision through the newly patched eye, failure to recover binocular vision, and a declining treatment efficacy with age (15, 17-21). Nevertheless, the success of reverse occlusion strategies demonstrates that severely weakened synaptic inputs in the brain can be rejuvenated under appropriate circumstances.An insight into how reverse occlusion might promote recovery came fr...

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Section: Discussionmentioning

confidence: 99%

Rapid recovery from the effects of early monocular deprivation is enabled by temporary inactivation of the retinas

Fong

Mitchell

Duffy

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…These silent synapses could later be 'unsilenced' or reactivated so as to permit subsequent, greatly enhanced levels of long-term potentiation (LTP) [69]. Another study using acute hippocampal slices showed similarly enhanced LTP after 3 h of TTX and APV (an NMDA receptor blocker) treatment [70]. Importantly, in vivo studies using sensory deprivation paradigms demonstrated that visual deprivation (i.e.…”

Section: Cellular and Molecular Mechanisms: Overlapping And Distinct mentioning

confidence: 99%

A metaplasticity view of the interaction between homeostatic and Hebbian plasticity

Yee¹,

Hsu²,

Chen³

2017

Phil. Trans. R. Soc. B

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One contribution of 16 to a discussion meeting issue 'Integrating Hebbian and homeostatic plasticity'. Hebbian and homeostatic plasticity are two major forms of plasticity in the nervous system: Hebbian plasticity provides a synaptic basis for associative learning, whereas homeostatic plasticity serves to stabilize network activity. While achieving seemingly very different goals, these two types of plasticity interact functionally through overlapping elements in their respective mechanisms. Here, we review studies conducted in the mammalian central nervous system, summarize known circuit and molecular mechanisms of homeostatic plasticity, and compare these mechanisms with those that mediate Hebbian plasticity. We end with a discussion of 'local' homeostatic plasticity and the potential role of local homeostatic plasticity as a form of metaplasticity that modulates a neuron's future capacity for Hebbian plasticity.This article is part of the themed issue 'Integrating Hebbian and homeostatic plasticity'.

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“…Moreover, following acoustic overexposure, fusiform cells that showed hyperactivity also exhibited a change in the firing pattern from regular spiking to bursting activity, a change that was mediated by a down regulation of high voltage activated potassium channels (Pilati et al, 2012). Because induction of LTP/LTD may depend on the cell’s intrinsic excitability (Felix-Oliveira et al, 2014), it is possible that such changes could contribute to the observed alterations in STDP plasticity following noise exposure and tinnitus.…”

Section: Multisensory Mechanisms In Cn and Their Contribution To Tmentioning

confidence: 99%

Tinnitus: Maladaptive auditory–somatosensory plasticity

Stefanescu

Martel

et al. 2016

Hearing Research

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Tinnitus, the phantom perception of sound, is physiologically characterized by an increase in spontaneous neural activity in the central auditory system. However, as tinnitus is often associated with hearing impairment, it is unclear how a decrease of afferent drive can result in central hyperactivity. In this review, we first assess methods for tinnitus induction and objective measures of the tinnitus percept in animal models. From animal studies, we discuss evidence that tinnitus originates in the cochlear nucleus (CN), and hypothesize mechanisms whereby hyperactivity may develop in the CN after peripheral auditory nerve damage. We elaborate how this process is likely mediated by plasticity of auditory-somatosensory integration in the CN: the circuitry in normal circumstances maintains a balance of auditory and somatosensory activities, and loss of auditory inputs alters the balance of auditory somatosensory integration in a stimulus timing dependent manner, which propels the circuit towards hyperactivity. Understanding the mechanisms underlying tinnitus generation is essential for its prevention and treatment.

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Homeostatic plasticity induced by brief activity deprivation enhances long-term potentiation in the mature rat hippocampus

Cited by 22 publications

References 58 publications

Rapid recovery from the effects of early monocular deprivation is enabled by temporary inactivation of the retinas

Rapid recovery from the effects of early monocular deprivation is enabled by temporary inactivation of the retinas

A metaplasticity view of the interaction between homeostatic and Hebbian plasticity

Tinnitus: Maladaptive auditory–somatosensory plasticity

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