Subcellular localization of the glutamate transporters GLAST and GLT at the neuromuscular junction in rodents

Rinholm, Johanne Egge; Slettaløkken, Gunnar; Marcaggi, Paı̈kan; Skare, Øivind; Storm‐Mathisen, Jon; Bergersen, Linda Hildegard

doi:10.1016/j.neuroscience.2006.12.041

Cited by 25 publications

(23 citation statements)

References 51 publications

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“…4 Recently, glutamate transporter 1 (GLT) has been shown to localize postsynaptically at NMJs in both rats and mice, while glutamate aspartate transporter (GLAST) has been shown to be restricted to rat NMJs. 32 This localization overlaps with our observed localization of the glutamate receptors. The localization of glutamate receptors, glutamate, and glutamate transporters suggest that a functional glutamatergic system is present at the mammalian NMJ.…”

Section: Discussionsupporting

confidence: 88%

Glutamate receptors localize postsynaptically at neuromuscular junctions in mice

et al. 2009

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Dlg (Discs Large) is a multidomain protein that interacts with glutamate receptors and potassium channels at Drosophila neuromuscular junctions (NMJs) and at mammalian central nervous system synapses. Dlg also localizes postsynaptically at cholinergic mammalian NMJs. We show here that α-amino-3-hydroxy-5-methylisoxazole-4-proprionate (AMPA) receptor subunits, together with glutamate, are present at the mammalian NMJ. Both AMPA and NMDA (N-methyl-D-aspartate) glutamate receptor subunits display overlapping postsynaptic localization patterns with Dlg at all NMJs examined in normal mice. Kir2 potassium channels also localize with Dlg and glutamate receptors at this synapse. Localization of the components of a glutamatergic system suggests novel mechanisms at mammalian neuromuscular synapses.

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Section: Discussionsupporting

confidence: 88%

Glutamate receptors localize postsynaptically at neuromuscular junctions in mice

et al. 2009

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“…The presence of glutamate transporter GLAST, which is localized mainly on the presynaptic membrane of Schwann cell, was revealed in experiments on the frog nerve-muscle preparation [80]. GLAST and GLT transporters were found in mammals in the area of endplate and they are fairly well represented in the synapses of both fast and slow muscles [93]. And it was established that most of them are localized deep in postsynaptic folds [93].…”

Section: Glutamatergic Signalingmentioning

confidence: 99%

“…GLAST and GLT transporters were found in mammals in the area of endplate and they are fairly well represented in the synapses of both fast and slow muscles [93]. And it was established that most of them are localized deep in postsynaptic folds [93].…”

Section: Glutamatergic Signalingmentioning

confidence: 99%

Non-Cholinergic Signaling Pathways at Vertebrate Neuromuscular Junctions

Malomouzh¹

2012

Skeletal Muscle - From Myogenesis to Clinical Relations

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“…57,58 While several regions have well characterized glutamate spillover between excitatory synapses, such as the cerebellum and hippocampus, there is ongoing debate regarding the extent of glutamate diffusion in other regions, including the frontal cortex, where spillover of glutamate may detrimentally lead to loss of input specificity and activation of cell death pathways. [59][60][61][62][63][64][65] Mathematical models suggest that glutamate may diffuse and activate NMDA receptors within a radius of 0.5 lm from the release point. 27 Thus, the spatial arrangement of glutamate synapses, their glutamate transporter buffering zones, and extrasynaptic glutamate receptors will determine the extent and effect of glutamate spillover.…”

Section: Extrasynaptic Glutamate Signalingmentioning

confidence: 99%

Glutamate Neurotransmission in Rodent Models of Traumatic Brain Injury

Dorsett

McGuire

DePasquale

et al. 2017

Journal of Neurotrauma

116

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Traumatic brain injury (TBI) is a leading cause of death and disability in people younger than 45 and is a significant public health concern. In addition to primary mechanical damage to cells and tissue, TBI involves additional molecular mechanisms of injury, termed secondary injury, that continue to evolve over hours, days, weeks, and beyond. The trajectory of recovery after TBI is highly unpredictable and in many cases results in chronic cognitive and behavioral changes. Acutely after TBI, there is an unregulated release of glutamate that cannot be buffered or cleared effectively, resulting in damaging levels of glutamate in the extracellular space. This initial loss of glutamate homeostasis may initiate additional changes in glutamate regulation. The excitatory amino acid transporters (EAATs) are expressed on both neurons and glia and are the principal mechanism for maintaining extracellular glutamate levels. Diffusion of glutamate outside the synapse due to impaired uptake may lead to increased extrasynaptic glutamate signaling, secondary injury through activation of cell death pathways, and loss of fidelity and specificity of synaptic transmission. Coordination of glutamate release and uptake is critical to regulating synaptic strength, long-term potentiation and depression, and cognitive processes. In this review, we will discuss dysregulation of extracellular glutamate and glutamate uptake in the acute stage of TBI and how failure to resolve acute disruptions in glutamate homeostatic mechanisms may play a causal role in chronic cognitive symptoms after TBI.

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Subcellular localization of the glutamate transporters GLAST and GLT at the neuromuscular junction in rodents

Cited by 25 publications

References 51 publications

Glutamate receptors localize postsynaptically at neuromuscular junctions in mice

Glutamate receptors localize postsynaptically at neuromuscular junctions in mice

Non-Cholinergic Signaling Pathways at Vertebrate Neuromuscular Junctions

Glutamate Neurotransmission in Rodent Models of Traumatic Brain Injury

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