Elimination of Inhibitory Synapses Is a Major Component of Adult Ocular Dominance Plasticity

Versendaal, Daniëlle van; Rajendran, Rajeev; Saiepour, M. Hadi; Klooster, Jan; Smit-Rigter, Laura A.; Sommeijer, Jean-Pierre; Zeeuw, Chris I. De; Hofer, Sonja B.; Heimel, J. Alexander; Levelt, Christiaan N.

doi:10.1016/j.neuron.2012.03.015

Cited by 196 publications

(216 citation statements)

References 46 publications

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“…Reducing the levels of inhibition onto excitatory neurons is consistently observed following loss of input in cortex [10,[22][23][24][25][26][27] and has been hypothesized to be a first step in circuit reorganization following input loss [28]. Changes in inhibition can occur via a reduction in the number [12,22,24,26,27,[29][30][31][32][33] or strength of inhibitory synapses onto excitatory cells [33], as well as a reduction in the firing rate of the inhibitory neurons following deprivation either temporarily during development [11,34] or for longer time courses in adulthood [29]. Changes in inhibitory tone may be modulated via astrocytes [35] or NMDA receptor input [36].…”

Section: Mechanisms Of Homeostatic Stabilizationmentioning

confidence: 99%

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

Keck

Toyoizumi

Chen

et al. 2017

Phil. Trans. R. Soc. B

184

192

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We summarize here the results presented and subsequent discussion from the meeting on Integrating Hebbian and Homeostatic Plasticity at the Royal Society in April 2016. We first outline the major themes and results presented at the meeting. We next provide a synopsis of the outstanding questions that emerged from the discussion at the end of the meeting and finally suggest potential directions of research that we believe are most promising to develop an understanding of how these two forms of plasticity interact to facilitate functional changes in the brain.This article is part of the themed issue 'Integrating Hebbian and homeostatic plasticity'.

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Section: Mechanisms Of Homeostatic Stabilizationmentioning

confidence: 99%

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

Keck

Toyoizumi

Chen

et al. 2017

Phil. Trans. R. Soc. B

184

192

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“…In utero electroporations were performed as described previously [38]. Plasmids drove expression of mito-mTurquoise2 and YFP-F (all adult in vivo experiments).…”

Section: In Utero Electroporationsmentioning

confidence: 99%

“…Cranial window implantation was performed as described [38]. For visualization of putative boutons and mitochondria in V1, animals (P90-P120) were anesthetized with ketamine and xylazine (100 mg/kg and 10 mg/kg i.p., respectively) and fixed on a magnetic head stage in the two-photon setup.…”

Section: In Vivo Two-photon Microscopy In Adult Micementioning

confidence: 99%

“…The lesions were 20 3 10 to 40 3 30 in size and localized dorsally above the optic disk. Six to eight days later, intrinsic-signal imaging to determine the lesioned area was performed as described [38]. So that a retinotopic map could be obtained, rectangular square-wave drifting gratings were presented four times for 6 s in each of 24 (6 3 4) equal squares on a liquid-crystal-display (LCD) screen, covering the visual field from À15 to +45 elevation and À15…”

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confidence: 99%

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Mitochondrial Dynamics in Visual Cortex Are Limited In Vivo and Not Affected by Axonal Structural Plasticity

et al. 2016

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[5] are often localized far away from the soma, mitochondria are actively transported to these sites [6][7][8][9][10][11]. Also, the removal and degradation of mitochondria are tightly regulated [9,12,13], because dysfunctional mitochondria are a source of reactive oxygen species, which can damage the cell [14]. Deficits in mitochondrial trafficking have been proposed to contribute to the pathogenesis of Parkinson's disease, schizophrenia, amyotrophic lateral sclerosis, optic atrophy, and Alzheimer's disease [13,[15][16][17][18][19]. In neuronal cultures, about a third of mitochondria are motile, whereas the majority remains stationary for several days [8,20]. Activity-dependent mechanisms cause mitochondria to stop at synaptic sites [7,8,20,21], which affects synapse function and maintenance. Reducing mitochondrial content in dendrites decreases spine density [22,23], whereas increasing mitochondrial content or activity increases it [7]. These bidirectional interactions between synaptic activity and mitochondrial trafficking suggest that mitochondria may regulate synaptic plasticity. Here we investigated the dynamics of mitochondria in relation to axonal boutons of neocortical pyramidal neurons for the first time in vivo. We find that under these circumstances practically all mitochondria are stationary, both during development and in adulthood. In adult visual cortex, mitochondria are preferentially localized at putative boutons, where they remain for several days. Retinal-lesion-induced cortical plasticity increases turnover of putative boutons but leaves mitochondrial turnover unaffected. We conclude that in visual cortex in vivo, mitochondria are less dynamic than in vitro, and that structural plasticity does not affect mitochondrial dynamics. RESULTS AND DISCUSSION Few Motile Mitochondria in Axons of Pyramidal Neurons in Visual Cortex In VivoTo fluorescently label mitochondria and the neuronal structures in which they are localized, we performed in utero electroporation with two DNA constructs driving expression of mitomTurquoise2 and membrane-associated YFP. A cranial window was implanted once mice had reached the age of 8-10 weeks. This allowed us to visualize mitochondria in axonal arbors of layer 2/3 pyramidal neurons in V1 in vivo using two-photon microscopy (Figures 1A-1C; Movie S1). Two to three weeks after cranial window implantation, optical imaging of intrinsic imaging was performed to localize monocular V1. One week later, axonal branches in layer 1 and upper layer 2 were imaged using in vivo two-photon microscopy. We found that the density of mitochondria was 0.09 per mm ( Figure 1D). Surprisingly, the fraction of axonal mitochondria that were motile was only 0.83% ( Figure 1E), much lower than the 10%-30% previously observed in neuronal cultures [6][7][8][9][10]. We therefore asked whether the difference in mitochondrial motility was caused by the different experimental condition (in vivo versus in vitro) or by the difference in the age of the imaged neurons. We assessed mitochondrial motilit...

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“…Dendritic spines are dynamic structures classically considered as excitatory postsynaptic sites. Intriguingly, dendritic spines are also emerging as inhibitory synaptic sites showing particularly high levels of plasticity 21,22 . Morphological plasticity of dendritic spines tightly correlates with the level of cortical plasticity 23,24 .…”

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confidence: 99%

Extracellular matrix inhibits structural and functional plasticity of dendritic spines in the adult visual cortex

et al. 2013

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Brain cells are immersed in a complex structure forming the extracellular matrix. The composition of the matrix gradually matures during postnatal development, as the brain circuitry reaches its adult form. The fully developed extracellular environment stabilizes neuronal connectivity and decreases cortical plasticity as highlighted by the demonstration that treatments degrading the matrix are able to restore synaptic plasticity in the adult brain. The mechanisms through which the matrix inhibits cortical plasticity are not fully clarified. Here we show that a prominent component of the matrix, chondroitin sulfate proteoglycans (CSPGs), restrains morphological changes of dendritic spines in the visual cortex of adult mice. By means of in vivo and in vitro two-photon imaging and electrophysiology, we find that after enzymatic digestion of CSPGs, cortical spines become more motile and express a larger degree of structural and functional plasticity.

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Elimination of Inhibitory Synapses Is a Major Component of Adult Ocular Dominance Plasticity

Cited by 196 publications

References 46 publications

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

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

Mitochondrial Dynamics in Visual Cortex Are Limited In Vivo and Not Affected by Axonal Structural Plasticity

Extracellular matrix inhibits structural and functional plasticity of dendritic spines in the adult visual cortex

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