Bidirectional Modifications of Visual Acuity Induced by Monocular Deprivation in Juvenile and Adult Rats

Iny, Karen; Heynen, Arnold J.; Sklar, E.; Bear, Mark F.

doi:10.1523/jneurosci.0124-06.2006

Cited by 50 publications

(60 citation statements)

References 51 publications

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“…In agreement with our findings, Iny et al (2006) found that BE produced partial recovery of behavioral acuity in adult rats. However, Pizzorusso et al (2006) reported little recovery in adult rats following 1 wk of RS.…”

supporting

confidence: 93%

Adult visual experience promotes recovery of primary visual cortex from long-term monocular deprivation

Fischer¹,

Aleem²,

Zhou³

et al. 2007

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Prolonged visual deprivation from early childhood to maturity is believed to cause permanent visual impairment. However, there have been case reports of substantial improvement of binocular vision in human adults following lifelong visual impairment or deprivation. These observations, together with recent findings of adult ocular dominance plasticity in rodents, led us to re-examine whether adult primary visual cortex (V1) is capable of any recovery following long-term monocular deprivation starting in development. Using mice as a model, we find that monocular deprivation from early development to mature ages (well past the critical period) severely impaired binocular vision by reducing the amplitude of responses elicited by stimulation of the deprived eye. Surprisingly, we find little effect on nondeprived eye responses. Restoration of binocular vision in mature adults yields modest but significant improvement of visual responses in V1. Remarkably, we find that when binocular vision is followed by occlusion of the nondeprived eye, visual responses in V1 recover almost fully, as measured by visual evoked potential amplitude, spatial frequency threshold, and single-unit activity. We conclude that adult V1 can recover from long-term deprivation when provided with an optimal regimen of visual experience.In comparison to the brain of children, the adult brain is thought to have a more limited capacity for regeneration and repair. One example of the decline of plasticity with age is the effect of monocular deprivation (MD). Classical electrophysiological studies found that early in life even a brief period of MD caused the visual cortex to respond very poorly to the deprived eye (in cats: Wiesel and Hubel 1963;Hubel and Wiesel 1970;Olson and Freeman 1975;Freeman and Olson 1982; in monkeys: Blakemore et al. 1978 in monkeys: Blakemore et al. , 1981 in rodents: Fagiolini et al. 1994;Gordon and Stryker 1996). Restoration of vision to the deprived eye can reverse the effect of MD only if the deprivation was brief. No recovery was observed after prolonged deprivation spanning a critical period of development (in cats: Wiesel and Hubel 1965;Hubel and Wiesel 1970;Blakemore and Van Sluyters 1974; in monkeys: Blakemore et al. 1978). These studies gave rise to the concept that disorders of central circuit development must be diagnosed and treated very early in childhood.Yet the adult brain appears to be more resilient and plastic than previously believed. A growing number of studies have found morphological and functional changes in motor and sensory neocortex as a result of altered experience or injury in adulthood (Merzenich et al. 1984;Jenkins et al. 1990;Allard et al. 1991;Fox 1992Fox , 1994Skibinska et al. 2000;Qi et al. 2000;Kaas and Qi 2004). Even in V1, our laboratory and others have found that ocular dominance (OD) plasticity exists in adult mice and rats (Guire et al. 1999;Sawtell et al. 2003;Pham et al. 2004;Lickey et al. 2004;Tagawa et al. 2005;Hofer et al. 2006;Fischer et al. 2007). These findings suggest the p...

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supporting

confidence: 93%

Adult visual experience promotes recovery of primary visual cortex from long-term monocular deprivation

Fischer¹,

Aleem²,

Zhou³

et al. 2007

Learn. Mem.

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“…Although our present findings provide direct evidence for the assumption that activity-dependent changes in the NR2A/NR2B ratio are involved in bidirectional metaplastic regulation of the LTP/LTD threshold (Bear, 2003;Iny et al, 2006;Philpot et al, 2007), we should keep in mind that there are probably many different mechanisms contributing to metaplasticity, as is also the case for synaptic plasticity [e.g., the observation that proportional but delayed NMDA potentiation after AMPA potentiation is the opposite of the prediction by the BCM theory, which predicts that LTP should reduce NMDA currents to raise the threshold for inducing subsequent LTP (Bienenstock et al, 1982;Watt et al, 2004)]. Therefore, although the BCM theory might have more generalized internal representations, the underlying mechanisms for LTP/LTD sliding could vary on a case-by-case basis.…”

Section: Metaplasticity Occurs When Pss Fail To Induce Persistent Chamentioning

confidence: 50%

“…A series of elegant investigations by Bear's laboratory in layer 3 of the visual cortex demonstrated that the "sliding threshold" is an attractive mechanism based on experience-dependent alterations in NMDARs (Kirkwood et al, 1996;Quinlan et al, 1999a,b;Philpot et al, 2001Philpot et al, , 2003Philpot et al, , 2007Shouval et al, 2002;Bear, 2003;Iny et al, 2006). The coincident alterations in the NR2A/NR2B ratio and in the LTP/LTD inspired the assumption that changes in NR2A/NR2B lead to sliding of LTP/LTD (Bear, 1995;Quinlan et al, 1999a,b;Philpot et al, 2007;Yashiro and Philpot, 2008).…”

Section: Introductionmentioning

confidence: 99%

Metaplastic Regulation of Long-Term Potentiation/Long-Term Depression Threshold by Activity-Dependent Changes of NR2A/NR2B Ratio

Chen²,

Gu³

et al. 2009

Journal of Neuroscience

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In vivo experience induces changes in synaptic NMDA receptor (NMDAR) subunit components, which are correlated with subsequent modifications of synaptic plasticity. However, little is known about how these subunit changes regulate the induction threshold of subsequent plasticity. At hippocampal Schaffer collateral-CA1 synapses, we first examined whether a recent history of neuronal activity could affect subsequent synaptic plasticity through its actions on NMDAR subunit components. We found that prior activity history produced by priming stimulations (PSs) across a wide range of frequencies (1-100 Hz) could induce bidirectional changes in the NR2A/NR2B ratio, which governs the threshold for subsequent long-term potentiation/long-term depression (LTP/LTD). Manipulating the NR2A/NR2B ratio through partial NR2 subunit blockade mimicked the PS regulation of the LTP/LTD threshold. Our results demonstrate that activity-dependent changes in the NR2A/NR2B ratio can be critical factors in metaplastic regulation of the LTP/LTD threshold.

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“…-Non-deprived eye response potentiation is behaviourally significant. Long-term MD leads to a gain in visual grating acuity through the non-deprived eye [67]. Of relevance to the upward drift in the deprived-eye response mentioned above, there is no evidence to our knowledge of any 'spontaneous' recovery of visual acuity through the deprived eye with prolonged deprivation.…”

Section: Ocular Dominance Plasticitymentioning

confidence: 98%

How the mechanisms of long-term synaptic potentiation and depression serve experience-dependent plasticity in primary visual cortex

Cooke

Bear

2014

Phil. Trans. R. Soc. B

108

115

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Donald Hebb chose visual learning in primary visual cortex (V1) of the rodent to exemplify his theories of how the brain stores information through long-lasting homosynaptic plasticity. Here, we revisit V1 to consider roles for bidirectional ‘Hebbian’ plasticity in the modification of vision through experience. First, we discuss the consequences of monocular deprivation (MD) in the mouse, which have been studied by many laboratories over many years, and the evidence that synaptic depression of excitatory input from the thalamus is a primary contributor to the loss of visual cortical responsiveness to stimuli viewed through the deprived eye. Second, we describe a less studied, but no less interesting form of plasticity in the visual cortex known as stimulus-selective response potentiation (SRP). SRP results in increases in the response of V1 to a visual stimulus through repeated viewing and bears all the hallmarks of perceptual learning. We describe evidence implicating an important role for potentiation of thalamo-cortical synapses in SRP. In addition, we present new data indicating that there are some features of this form of plasticity that cannot be fully accounted for by such feed-forward Hebbian plasticity, suggesting contributions from intra-cortical circuit components.

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Bidirectional Modifications of Visual Acuity Induced by Monocular Deprivation in Juvenile and Adult Rats

Cited by 50 publications

References 51 publications

Adult visual experience promotes recovery of primary visual cortex from long-term monocular deprivation

Adult visual experience promotes recovery of primary visual cortex from long-term monocular deprivation

Metaplastic Regulation of Long-Term Potentiation/Long-Term Depression Threshold by Activity-Dependent Changes of NR2A/NR2B Ratio

How the mechanisms of long-term synaptic potentiation and depression serve experience-dependent plasticity in primary visual cortex

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