Co‐regulation of ocular dominance plasticity and NMDA receptor subunit expression in glutamic acid decarboxylase‐65 knock‐out mice

Kanold, Patrick O.; Kim, Yoon A; GrandPré, Tadzia; Shatz, Carla J.

doi:10.1113/jphysiol.2009.171215

Cited by 34 publications

(49 citation statements)

References 59 publications

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“…To test whether the prolonged sensitive phase for OD plasticity in our EE mice was mediated by a reduced GABAergic inhibition in V1, which was suggested for rat visual cortex (18,19,21), we used two different paradigms. First, we measured intracortical inhibition directly by in vitro patch-clamp electrophysiology in V1 slices from adult (>PD130) EE and SC mice, and second, we boosted GABAergic inhibition in vivo by injecting diazepam (22,23) to test whether diazepam would prevent OD plasticity after MD. Juvenile level of inhibition in adult EE mice.…”

mentioning

confidence: 99%

Environmental enrichment extends ocular dominance plasticity into adulthood and protects from stroke-induced impairments of plasticity

Greifzu

Pielecka-Fortuna

Kalogeraki

et al. 2014

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

136

208

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Ocular dominance (OD) plasticity in mouse primary visual cortex (V1) declines during postnatal development and is absent beyond postnatal day 110 if mice are raised in standard cages (SCs). An enriched environment (EE) promotes OD plasticity in adult rats. Here, we explored cellular mechanisms of EE in mouse V1 and the therapeutic potential of EE to prevent impairments of plasticity after a cortical stroke. Using in vivo optical imaging, we observed that monocular deprivation in adult EE mice (i) caused a very strong OD plasticity previously only observed in 4-wk-old animals, (ii) restored already lost OD plasticity in adult SC-raised mice, and (iii) preserved OD plasticity after a stroke in the primary somatosensory cortex. Using patch-clamp electrophysiology in vitro, we also show that (iv) local inhibition was significantly reduced in V1 slices of adult EE mice and (v) the GABA/AMPA ratio was like that in 4-wk-old SC-raised animals. These observations were corroborated by in vivo analyses showing that diazepam treatment significantly reduced the OD shift of EE mice after monocular deprivation. Taken together, EE extended the sensitive phase for OD plasticity into late adulthood, rejuvenated V1 after 4 mo of SCrearing, and protected adult mice from stroke-induced impairments of cortical plasticity. The EE effect was mediated most likely by preserving low juvenile levels of inhibition into adulthood, which potentially promoted adaptive changes in cortical circuits. O cular dominance (OD) plasticity induced by monocular deprivation (MD) is one of the best studied models of experience-dependent plasticity in the mammalian cortex (1, 2). OD plasticity in primary visual cortex (V1) of C57BL/6J mice is maximal at 4 wk of age, declines after 2-3 mo, and is absent beyond postnatal day 110 (PD110) if animals are raised in standard cages (SCs) (3-6). In 4-wk-old mice, 4 d of MD are sufficient to induce an OD shift to the open eye; therefore, neurons in the binocular V1, which are usually dominated by the contralateral eye in rodents (3, 7), become activated more equally by both eyes (5,8). This juvenile OD shift is predominantly mediated by a decrease in the visual cortical responses to the deprived eye (1, 9-11), whereas significant OD shifts in older animals up to PD110 need 7 d of MD and are mediated primarily by increased openeye responses in V1. Raising animals in an enriched environment (EE) gives them the opportunity of enhanced physical, social, and cognitive stimulation and influences brain physiology and behavior in many ways (12, 13). It has been shown previously that EE enhances visual system development in rats (14) and mice (15-17), increases levels of the brain-derived neurotrophic factor and serotonin (18), reduces both extracellular GABA levels (18, 19) and the density of ECM perineuronal nets (PNNs) (19), and promotes OD plasticity in adult and aging rats (18-21). Here, we explored cellular mechanisms of EE in V1 of mice and the therapeutic potential of EE to prevent impairments of plasticity after a c...

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mentioning

confidence: 99%

Environmental enrichment extends ocular dominance plasticity into adulthood and protects from stroke-induced impairments of plasticity

Greifzu

Pielecka-Fortuna

Kalogeraki

et al. 2014

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

136

208

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“…ticity and LTD and causes deregulation of NMDA receptor levels (16,31,44). We show that removal of Cx36 impairs OD plasticity and LTP.…”

Section: Discussionmentioning

confidence: 96%

“…To explore this issue, we measured the expression of Arc, an immediate early gene that is rapidly expressed in visual cortical neurons after brief visual stimulation (11,(29)(30)(31) with in situ hybridization. The visually induced expression pattern of Arc is a sensitive indicator of OD plasticity in both mice and cats (11,(29)(30)(31). As expected, after monocular enucleation (ME) in control, the functional representation of the NDE increased in control (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…OD ratio was computed as contra/ipsi VEP amplitude ratio. OD plasticity experiments using Arc and qRT-PCR were carried out as described (11,(29)(30)(31)48). ANOVA, t test, or Wilcoxon was used for statistical comparisons, and P < 0.05 was considered significant.…”

Section: Methodsmentioning

confidence: 99%

“…Cx36KO mice were generated as described (6). Slice electrophysiology was performed as described (24,31). To record EPSCs, pipettes were filled with a cesium-based solution.…”

Section: Methodsmentioning

confidence: 99%

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Electrical synapses formed by connexin36 regulate inhibition- and experience-dependent plasticity

Postma

Liu²,

Dietsche³

et al. 2011

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

Self Cite

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The mammalian brain constantly adapts to new experiences of the environment, and inhibitory circuits play a crucial role in this experience-dependent plasticity. A characteristic feature of inhibitory neurons is the establishment of electrical synapses, but the function of electrical coupling in plasticity is unclear. Here we show that elimination of electrical synapses formed by connexin36 altered inhibitory efficacy and caused frequency facilitation of inhibition consistent with a decreased GABA release in the inhibitory network. The altered inhibitory efficacy was paralleled by a failure of theta-burst long-term potentiation induction and by impaired ocular dominance plasticity in the visual cortex. Together, these data suggest a unique mechanism for regulating plasticity in the visual cortex involving synchronization of inhibitory networks via electrical synapses.gap junctions | development | cannabinoid receptor 1 | synchrony S ynaptic interactions in the mammalian brain are sculpted by experience, particularly during "critical periods" in development. Accumulating evidence suggests that inhibitory neurons play a crucial role in reshaping neural networks in response to sensory perturbations (1). Inhibitory neurons in many areas of the brain, including the cerebral cortex, are coupled via gap junctions containing connexin36 (Cx36), which allow subthreshold fluctuations in membrane potential to spread between cells and promote synchrony of firing (2-5). Cx36-null mice (Cx36KO) display decreased coherence of rhythmic activity in populations of cortical interneurons in brain slices and decreased strength of evoked cortical inhibition in vivo (6-8). Similar effects of Cx36 signaling might underlie the behavioral deficits in cerebellar learning tasks in Cx36KO (7). However, the possible functions of Cx36 in sensory cortical development and plasticity are unknown.A common model for experience-dependent synaptic modification is ocular dominance (OD) plasticity of visual cortex. In the visual cortex, decreasing neural activity in one eye (monocular deprivation; MD) leads to weakening and removal of connections representing the deprived eye (DE) and strengthening and expansion of connections representing the nondeprived eye (NDE; refs. 9-13). These manipulations are particularly effective during the critical period, which extends from postnatal day (P) 19 to ∼P55 and peaks at ∼P25-28 in mice (11,14,15). Both inhibition and synaptic plasticity mechanisms, such as long-term potentiation (LTP) and long-term depression (LTD), play a key role in OD plasticity, and inhibition can alter synaptic plasticity (1,16,17). Cx36 is present in most cortical layers during the critical period for OD plasticity (6). We therefore investigated to what degree Cx36 controls inhibitory function and, consequently, synaptic and OD plasticity.Here we report altered dynamics of the evoked inhibitory synaptic currents in mice lacking Cx36, such that there is a reduction when probed at low-frequency stimulation but a facilitation at higher frequ...

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Ocular dominance plasticity: Molecular mechanisms revisited

Kasamatsu

Imamura

2020

J of Comparative Neurology

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Ocular dominance plasticity (ODP) is a type of cortical plasticity operating in visual cortex of mammals that are endowed with binocular vision based on the competition-driven disparity. Earlier, a molecular mechanism was proposed that catecholamines play an important role in the maintenance of ODP in kittens. Having survived the initial test, the hypothesis was further advanced to identify noradrenaline (NA) as a key factor that regulates ODP in the immature cortex. Later, the ODPpromoting effect of NA is extended to the adult with age-related limitations. Following the enhanced NA availability, the chain events downstream lead to the β-adrenoreceptor-induced cAMP accumulation, which in turn activates the protein kinase A. Eventually, the protein kinase translocates to the cell nucleus to activate cAMP responsive element binding protein (CREB). CREB is a cellular transcription factor that controls the transcription of various genes, underpinning neuronal plasticity and long-term memory. In the advent of molecular genetics in that various types of new tools have become available with relative ease, ODP research has lightly adopted in the rodent model the original concepts and methodologies. Here, after briefly tracing the strategic maturation of our quest, the review moves to the later development of the field, with the emphasis placed around the following issues: (a) Are we testing ODP per se? (b) What does monocular deprivation deprive of the immature cortex? (c) The critical importance of binocular competition, (d) What is the adult plasticity? (e) Excitation-Inhibition balance in local circuits, and (f) Species differences in the animal models.

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Co‐regulation of ocular dominance plasticity and NMDA receptor subunit expression in glutamic acid decarboxylase‐65 knock‐out mice

Cited by 34 publications

References 59 publications

Environmental enrichment extends ocular dominance plasticity into adulthood and protects from stroke-induced impairments of plasticity

Environmental enrichment extends ocular dominance plasticity into adulthood and protects from stroke-induced impairments of plasticity

Electrical synapses formed by connexin36 regulate inhibition- and experience-dependent plasticity

Ocular dominance plasticity: Molecular mechanisms revisited

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