Neural mechanisms of recovery following early visual deprivation

Mitchell, Donald E.; Sengpiel, Frank

doi:10.1098/rstb.2008.0192

Cited by 57 publications

(48 citation statements)

References 110 publications

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“…The range and average age of the mice for each subgroup were as follows: WT no MD: age range: 1.9 -3.5 months, average 2.8 months, WT MD: age range 1.7-10.5 months, average 4.8 months, Lynx1 KO no MD: 4 -7.5 months, average 6.4 months, Lynx1 KO MD: 2.8 -7.4 months, average: 5.3 months, DKO no MD: 2.5-4.2 months, average: 3.2 months, and DKO MD: 2.5-4 months, average 3.6 months. All mice but one WT no MD mouse and two WT MD mice were older than P72, when no OD plasticity is detected after 4 d of MD (Stodieck et al, 2014). Among WT mice with MD, there was no statistically significant difference in OD plasticity (CBI) between adult mice group younger than P72 (2 mice) versus mice group older than P72 (5 mice) ( p ϭ 0.599, t test), or between adult mice younger than P110 (3 mice) versus fully adult mice older than P110 (4 mice) subgroups ( p ϭ 0.253, t test).…”

Section: Tpa Is Required For the Elevated Od Plasticity In Adult Lynxmentioning

confidence: 99%

“…The range and the average age of mice for each subgroup were as follows: WT no MD: 2.6 -6.8 months, average 6.1 months, WT MD: 2.6 -6.8 months, average 4.7 months, Lynx1 KO no MD: 2.4 -13.1 months, average 8.1 months, and Lynx1 KO MD: 2.3-11.0 months, average 5.9 months. As a recent study reported, no significant OD plasticity in WT mice ϳP72 (age range P57-P80) (Stodieck et al, 2014), we also compared the tPA activity only with the mice older than P72 (excluding 2 mice each from KO noMD group and KO MD group who were younger than P72). In these sets of mice over P72, Lynx1KO MD groups (14 mice) maintained a statistically significant increase in tPA activity compared with age-matched controls ( p ϭ 0.031 vs WT MD group, 12 mice; p ϭ 0.020 vs Lynx1 KO no MD group, 16 mice, t test).…”

Section: Tpa Activity Elevates In Adult V1 Following MD In Lynx1 Ko Micementioning

confidence: 99%

“…Importantly, such juvenile forms of plasticity become limited in adult V1 under standard housing conditions. However, OD plasticity can be either reactivated or preserved even in the adult with additional environmental, such as dark exposure (He et al, 2006(He et al, , 2007Duffy and Mitchell, 2013;Stodieck et al, 2014), environmental enrichment (Sale et al, 2007;Greifzu et al, 2014), visual stimulation (Matthies et al, 2013), sensory-motor interaction (Kaneko and Stryker, 2014;Fu et al, 2015), voluntary physical exercise (Kalogeraki et al, 2014), and social experience (Balog et al, 2014) in addition to pharmacological interventions (Putignano et al, 2007;Morishita et al, 2010;Nabel and Morishita, 2013), suggesting the intrinsic potential of the adult brain to unmask plasticity. Although there is significant progress in determining the underlying neural mechanisms of interventions, such as reduced intracortical inhibition Stodieck et al, 2014), disinhibitory cortical circuit (Fu et al, 2015), and serotonin (Matthies et al, 2013), it is essential to keep uncovering molecular bases of such intrinsic potential of adult V1 to promote plasticity and understand how such potentials can be unmasked in adult V1.…”

Section: Introductionmentioning

confidence: 99%

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Unmasking Proteolytic Activity for Adult Visual Cortex Plasticity by the Removal of Lynx1

et al. 2015

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Experience-dependent cortical plasticity declines with age. At the molecular level, experience-dependent proteolytic activity of tissue plasminogen activator (tPA) becomes restricted in the adult brain if mice are raised in standard cages. Understanding the mechanism for the loss of permissive proteolytic activity is therefore a key link for improving function in adult brains. Using the mouse primary visual cortex (V1) as a model, we demonstrate that tPA activity in V1 can be unmasked following 4 d of monocular deprivation when the mice older than 2 months are raised in standard cages by the genetic removal of Lynx1, a negative regulator of adult plasticity. This was also associated with the reduction of stubby and thin spine density and enhancement of ocular dominance shift in adult V1 of Lynx1 knock-out (KO) mice. These structural and functional changes were tPA-dependent because genetic removal of tPA in Lynx1 KO mice can block the monocular deprivation-dependent reduction of dendritic spine density, whereas both genetic and adult specific inhibition of tPA activity can ablate the ocular dominance shift in Lynx1 KO mice. Our work demonstrates that the adult brain has an intrinsic potential for experience-dependent elevation of proteolytic activity to express juvenile-like structural and functional changes but is effectively limited by Lynx1 if mice are raised in standard cages. Insights into the Lynx1-tPA plasticity mechanism may provide novel therapeutic targets for adult brain disorders.

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Section: Tpa Is Required For the Elevated Od Plasticity In Adult Lynxmentioning

confidence: 99%

Section: Tpa Activity Elevates In Adult V1 Following MD In Lynx1 Ko Micementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Unmasking Proteolytic Activity for Adult Visual Cortex Plasticity by the Removal of Lynx1

et al. 2015

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“…Recent experiments have shown that the reduction of responses from the deprived eye occurs rapidly, followed by a slower increase of drive from the nondeprived eye (6,7). Recovery of deprived eye responses after eye reopening occurs robustly (8,9), although its time course has not been well studied.…”

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confidence: 99%

Rapid experience-dependent plasticity of synapse function and structure in ferret visual cortex in vivo

Majewska

Sur

2011

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

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The rules by which visual experience influences neuronal responses and structure in the developing brain are not well understood. To elucidate the relationship between rapid functional changes and dendritic spine remodeling in vivo, we carried out chronic imaging experiments that tracked visual responses and dendritic spines in the ferret visual cortex following brief periods of monocular deprivation. Functional changes, which were largely driven by loss of deprived eye responses, were tightly regulated with structural changes at the level of dendritic spines, and occurred very rapidly (on a timescale of hours). The magnitude of functional changes was correlated with the magnitude of structural changes across the cortex, and both these features reversed when the deprived eye was reopened. A global rule governed how the responses to the two eyes or changes in spines were altered by monocular deprivation: the changes occurred irrespective of regional ocular dominance preference and were independently mediated by each eye, and the loss or gain of responses/spines occurred as a constant proportion of predeprivation drive by the deprived or nondeprived eye, respectively. cortical circuits | ocular dominance plasticity | optical imaging | two-photon imaging E xperience-dependent plasticity in the primary visual cortex (i.e., V1) is a proving ground for understanding how the quality and quantity of input activity influences cortical synapses and circuits. In particular, blocking or reducing activity in one eye during a critical period of development leads to a physiological loss of responses to stimulation of the deprived eye and an increase of responses to the nondeprived eye (1, 2). The dynamics of ocular dominance (OD) plasticity are key to understanding its mechanisms. Initial estimates (2) suggested that functional changes in OD preference could occur with 3 to 6 d of monocular deprivation (MD). Subsequent experiments demonstrated that a saturating functional shift of OD preference required several days of MD at the peak of the critical period (3, 4). However, a significant reduction in deprived eye responses can be recorded even after a few hours of deprivation (5). Recent experiments have shown that the reduction of responses from the deprived eye occurs rapidly, followed by a slower increase of drive from the nondeprived eye (6, 7). Recovery of deprived eye responses after eye reopening occurs robustly (8, 9), although its time course has not been well studied.The structural basis of OD plasticity has also been studied at different timescales, but the mechanisms for rapid loss and recovery of responses remain unresolved. Several weeks of MD in cats leads to a shrinkage of deprived eye thalamocortical arbors and an expansion of nondeprived eye arbors (10, 11). However, 2 d of MD has no effect on the relative numerical synaptic density or synaptic vesicle protein density in deprived and nondeprived afferents (12). In contrast, 7 d of MD causes a decrease in the total length of deprived-eye geniculocortical arbors...

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“…It therefore follows that deprivation or overloading of a certain sensory experience may affect the function of those receiving brain regions [9]. It is well-known that visual deprivation promotes the somatosensory or auditory system in animal models as well as in humans [10]. Especially, the abnormal sensory stimulation in the early life (e. g. juvenile and adolescent periods) can disturb the normal structure and function of brain circuits [11,12].…”

Section: Introductionmentioning

confidence: 99%

Effects of Saccharin Intake on Hippocampal and Cortical Plasticity in Juvenile and Adolescent Rats

Park

Yoo

Kim

et al. 2010

Korean J Physiol Pharmacol

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The sensory system is developed and optimized by experiences given in the early phase of life in association with other regions of the nervous system. To date, many studies have revealed that deprivation of specific sensory experiences can modify the structure and function of the central nervous system; however, the effects of sensory overload remains unclear. Here we studied the effect of overloading the taste sense in the early period of life on the synaptic plasticity of rat hippocampus and somatosensory cortex. W e prepared male and female Sprague Dawley rats with ad libitum access to a 0.1% saccharin solution for 2 hrs per day for three weeks after weaning on postnatal day 22. Saccharin consumption was slightly increased in males compared with females; however, saccharin intake did not affect chow intake or weight gain either in male or in female rats. W e examined the effect of saccharin-intake on long term potentiation (LTP) formation in hippocampal Schaffer collateral pathway and somatosensory cortex layer IV -II/III pathways in the 6-week old saccharin-fed rats. There was no significant difference in LTP formation in the hippocampus between the control group and saccharin-treated group in both male and female rats. Also in the somatosensory cortex, we did not see a significant difference in LTP among the groups. Therefore, we conclude that saccharin-intake during 3∼ 6 weeks may not affect the development of physiological function of the cortical and hippocampal synapses in rats.

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Neural mechanisms of recovery following early visual deprivation

Cited by 57 publications

References 110 publications

Unmasking Proteolytic Activity for Adult Visual Cortex Plasticity by the Removal of Lynx1

Unmasking Proteolytic Activity for Adult Visual Cortex Plasticity by the Removal of Lynx1

Rapid experience-dependent plasticity of synapse function and structure in ferret visual cortex in vivo

Effects of Saccharin Intake on Hippocampal and Cortical Plasticity in Juvenile and Adolescent Rats

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