Glutamate Transporters Regulate Lesion-Induced Plasticity in the Developing Somatosensory Cortex

Takasaki, Chihiro; Okada, Rieko; Mitani, Akira; Fukaya, Masahiro; Yamasaki, Miwako; Fujihara, Yuri; Shirakawa, Tetsuo; Tanaka, Kohichi; Watanabe, Masahiko

doi:10.1523/jneurosci.0861-08.2008

Cited by 48 publications

(54 citation statements)

References 92 publications

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“…10 A, available at www.jneurosci.org as supplemental material). When ION transection was performed on P2 mice, barrel formation was effectively disrupted (data not shown) as described previously (Takasaki et al, 2008), suggesting that the surgical procedure itself had been done successfully. Together, these results suggest that neuronal activity is dispensable for the formation of whisker-related patterns of barrel nets.…”

Section: Reorganization Of Barrel Nets Induced By Cauterization Of Whsupporting

confidence: 74%

“…10 A, available at www.jneurosci.org as supplemental material). Mice were subjected to ION transection at P5 so that the input from the whisker pad was totally blocked, while whisker-related patterns of barrels were left intact (Takasaki et al, 2008). When examined at P15, whisker-related patterns of barrel nets were readily observable (supplemental Fig.…”

Section: Reorganization Of Barrel Nets Induced By Cauterization Of Whmentioning

confidence: 99%

See 1 more Smart Citation

Whisker-Related Axonal Patterns and Plasticity of Layer 2/3 Neurons in the Mouse Barrel Cortex

Sehara

Toda²,

Iwai³

et al. 2010

J. Neurosci.

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Elucidating neuronal circuits and their plasticity in the cerebral cortex is one of the important questions in neuroscience research. Here we report novel axonal trajectories and their plasticity in the mouse somatosensory barrel cortex. We selectively visualized layer 2/3 neurons using in utero electroporation and examined the axonal trajectories of layer 2/3 neurons. We found that the axons of layer 2/3 neurons preferentially run in the septal regions of layer 4 and named this axonal pattern "barrel nets." The intensity of green fluorescent protein in the septal regions was markedly higher compared with that in barrel hollows. Focal in utero electroporation revealed that the axons in barrel nets were indeed derived from layer 2/3 neurons in the barrel cortex. During development, barrel nets became visible at postnatal day 10, which was well after the initial appearance of barrels. When whisker follicles were cauterized within 3 d after birth, the whisker-related pattern of barrel nets was altered, suggesting that cauterization of whisker follicles results in developmental plasticity of barrel nets. Our results uncover the novel axonal trajectories of layer 2/3 neurons with whisker-related patterns and their developmental plasticity in the mouse somatosensory cortex. Barrel nets should be useful for investigating the pattern formation and axonal reorganization of intracortical neuronal circuits.

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Section: Reorganization Of Barrel Nets Induced By Cauterization Of Whsupporting

confidence: 74%

Section: Reorganization Of Barrel Nets Induced By Cauterization Of Whmentioning

confidence: 99%

Whisker-Related Axonal Patterns and Plasticity of Layer 2/3 Neurons in the Mouse Barrel Cortex

Sehara

Toda²,

Iwai³

et al. 2010

J. Neurosci.

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“…When whiskers are damaged during the critical period, lesioned barrels shrink and adjacent intact barrels expand (46). Intriguingly, the magnitude of this lesion-induced plasticity is diminished severely in GLT-1-KO mice, and mildly in GLAST-KO mice (47). Because whiskerrelated patterning is regulated by the NMDA-type glutamate receptor and the mGluR5-PLCβ1 signaling pathway (48)(49)(50), elevated [Glu] e in the somatosensory cortex may also impair the discrimination of activity disparity among glutamatergic inputs.…”

Section: Discussionmentioning

confidence: 99%

Glutamate transporter GLAST controls synaptic wrapping by Bergmann glia and ensures proper wiring of Purkinje cells

Miyazaki

Yamasaki

Hashimoto

et al. 2017

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

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Astrocytes regulate synaptic transmission through controlling neurotransmitter concentrations around synapses. Little is known, however, about their roles in neural circuit development. Here we report that Bergmann glia (BG), specialized cerebellar astrocytes that thoroughly enwrap Purkinje cells (PCs), are essential for synaptic organization in PCs through the action of the L-glutamate/L-aspartate transporter (GLAST). In GLAST-knockout mice, dendritic innervation by the main ascending climbing fiber (CF) branch was significantly weakened, whereas the transverse branch, which is thin and nonsynaptogenic in control mice, was transformed into thick and synaptogenic branches. Both types of CF branches frequently produced aberrant wiring to proximal and distal dendrites, causing multiple CF-PC innervation. Our electrophysiological analysis revealed that slow and small CF-evoked excitatory postsynaptic currents (EPSCs) were recorded from almost all PCs in GLAST-knockout mice. These atypical CF-EPSCs were far more numerous and had significantly faster 10-90% rise time than those elicited by glutamate spillover under pharmacological blockade of glial glutamate transporters. Innervation by parallel fibers (PFs) was also affected. PF synapses were robustly increased in the entire dendritic trees, leading to impaired segregation of CF and PF territories. Furthermore, lamellate BG processes were retracted from PC dendrites and synapses, leading to the exposure of these neuronal elements to the extracellular milieus. These synaptic and glial phenotypes were reproduced in wild-type mice after functional blockade of glial glutamate transporters. These findings highlight that glutamate transporter function by GLAST on BG plays important roles in development and maintenance of proper synaptic wiring and wrapping in PCs.glutamate transporter | Purkinje cell | Bergmann glia | climbing fiber | parallel fiber

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“…Homozygote EAAT2-knockout mice (Tanaka et al, 1997) are inconspicuous at birth because EAAT2 expression is very low in newborn rats and mice (Ullensvang et al, 1997;Furuta et al, 1997;Hanson et al, 2015), but they become spontaneously epileptic at around three weeks of age and about half of them have died by the end of the fourth week (Tanaka et al, 1997;Mitani and Tanaka, 2003;Takasaki et al, 2008). A selective deletion of EAAT2 in the brain is sufficient to reproduce this phenotype confirming that EAAT2 plays its most important role in the brain (Zhou et al, 2014b).…”

Section: Eaat2mentioning

confidence: 97%

Neuronal vs glial glutamate uptake: Resolving the conundrum

Danbolt

Furness

Zhou

2016

Neurochemistry International

186

152

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Neither normal brain function nor the pathological processes involved in neurological diseases can be adequately understood without knowledge of the release, uptake and metabolism of glutamate. The reason for this is that glutamate (a) is the most abundant amino acid in the brain, (b) is at the cross-roads between several metabolic pathways, and (c) serves as the major excitatory neurotransmitter. In fact most brain cells express glutamate receptors and are thereby influenced by extracellular glutamate. In agreement, brain cells have powerful uptake systems that constantly remove glutamate from the extracellular fluid and thereby limit receptor activation. It has been clear since the 1970s that both astrocytes and neurons express glutamate transporters. However, the relative contribution of neuronal and glial transporters to the total glutamate uptake activity, however, as well as their functional importance, has been hotly debated ever since. The present short review provides (a) an overview of what we know about neuronal glutamate uptake as well as an historical description of how we got there, and (b) a hypothesis reconciling apparently contradicting observations thereby possibly resolving the paradox. ABBREVIATIONSCre, Cyclization recombinase (Le and Sauer, 2000); EAAC1, glutamate transporter (EAAT3; slc1a1; Kanai and Hediger, 1992; Bjørås et al., 1996); EAAT, excitatory amino acid transporter (synonym to glutamate transporter); GABA, γ-aminobutyric acid; GLAST, rat glutamate transporter (EAAT1; slc1a3; Storck et al., 1992;Tanaka, 1993a); GLT-1, rat glutamate transporter (EAAT2; slc1a2; Pines et al., 1992); GLUL, glutamine synthetase; TBOA, DL-threo-β-benzyloxyaspartate AbstractNeither normal brain function nor the pathological processes involved in neurological diseases can be adequately understood without knowledge of the release, uptake and metabolism of glutamate. The reason for this is that glutamate (a) is the most abundant amino acid in the brain, (b) is at the cross-roads between several metabolic pathways, and (c) serves as the major excitatory neurotransmitter. In fact most brain cells express glutamate receptors and are thereby influenced by extracellular glutamate. In agreement, brain cells have powerful uptake systems that constantly remove glutamate from the extracellular fluid and thereby limit receptor activation. It has been clear since the 1970s that astrocytes and neurons express glutamate transporters. The relative contribution of neuronal and glial transporters to the total glutamate uptake activity, however, as well as their functional importance, has been hotly debated ever since. The present short review provides (a) an overview of what we know about neuronal glutamate uptake as well as an historical description of how we got there, and (b) an hypothesis reconciling apparently contradicting observations thereby possibly resolving the paradox.

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Glutamate Transporters Regulate Lesion-Induced Plasticity in the Developing Somatosensory Cortex

Cited by 48 publications

References 92 publications

Whisker-Related Axonal Patterns and Plasticity of Layer 2/3 Neurons in the Mouse Barrel Cortex

Whisker-Related Axonal Patterns and Plasticity of Layer 2/3 Neurons in the Mouse Barrel Cortex

Glutamate transporter GLAST controls synaptic wrapping by Bergmann glia and ensures proper wiring of Purkinje cells

Neuronal vs glial glutamate uptake: Resolving the conundrum

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