Enhanced neuronal death from focal ischemia in AMPA-receptor transgenic mice

Le, Dean A.; Das, Saumya; Wang, Yanming F.; Yoshizawa, Toshihiro; Sasaki, Y.; Takasu, Mari A.; Nemes, Adriana; Mendelsohn, Monica; Dikkes, Pieter; Lipton, Stuart A.; Nakanishi, Norihiko

doi:10.1016/s0169-328x(97)00261-1

Cited by 32 publications

(16 citation statements)

References 21 publications

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“…Studies of mice overexpressing GluR2 indicate that excitotoxic vulnerability increases as the abundance of AMPA receptors increases (Le et al, 1997). For neurons possessing comparable AMPA receptor abundance, those expressing lower levels of GluR2 tend to be more vulnerable (Pellegrini-Giampietro et al, 1992Feldmeyer et al, 1999;Iihara et al, 2001).…”

Section: Projection Neurons Versus Interneurons-thementioning

confidence: 99%

Differential localization of the GluR1 and GluR2 subunits of the AMPA-type glutamate receptor among striatal neuron types in rats

Deng

Xie

Wang

et al. 2007

Journal of Chemical Neuroanatomy

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Differences among the various striatal projection neuron and interneuron types in cortical input, function, and vulnerability to degenerative insults may be related to differences among them in AMPA-type glutamate receptor abundance and subunit configuration. We therefore used immunolabeling to assess the frequency and abundance of GluR1 and GluR2, the most common AMPA subunits in striatum, in the main striatal neuron types. All neurons projecting to the external pallidum (GPe), internal pallidum (GPi) or substantia nigra, as identified by retrograde labeling, possessed perikaryal GluR2, while GluR1 was more common in striato-GPe than striato-GPi perikarya. The frequency and intensity of immunostaining indicated the rank order of their perikaryal GluR1:GluR2 ratio to be striato-GPe > striatonigral > striato-GPi. Ultrastructural studies suggested a differential localization of GluR1 and GluR2 to striatal projection neuron dendritic spines as well, with GluR1 seemingly more common in striato-GPe spines and GluR2 more common in striato-GPi and/or striatonigral spines. Comparisons among projection neurons and interneurons revealed GluR1 to be most common and abundant in parvalbuminergic interneurons, and GluR2 most common and abundant in projection neurons, with the rank order for the GluR1:GluR2 ratio being parvalbuminergic interneurons > calretinergic interneurons > cholinergic interneurons > projection neurons > somatostatinergic interneurons. Striosomal projection neurons had a higher GluR1:GluR2 ratio than did matrix projection neurons. The abundance of both GluR1 and GluR2 in striatal parvalbuminergic interneurons and projection neurons is consistent with their prominent cortical input and susceptibility to excitotoxic insult, while differences in GluR1: GluR2 ratio among projection neurons are likely to yield differences in Ca2+ permeability, desensitization, and single channel current, which may contribute to differences among them in plasticity, synaptic integration, and excitotoxic vulnerability. The apparent association of the GluR1 subunit with synaptic plasticity, in particular, suggests striato-GPe neuron spines as a particular site of corticostriatal synaptic plasticity, presumably associated with motor learning.

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Section: Projection Neurons Versus Interneurons-thementioning

confidence: 99%

Differential localization of the GluR1 and GluR2 subunits of the AMPA-type glutamate receptor among striatal neuron types in rats

Deng

Xie

Wang

et al. 2007

Journal of Chemical Neuroanatomy

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“…These findings, as well as previous reports (Tancredi et al, 1992;Grassi et al, 1994;Emch et al, 2000), suggest that TNF␣ can have significant effects on neural circuit function. Furthermore, the TNF␣-induced increase in the surface expression of AMPARs may contribute significantly to its putative role in mediating the brain damage resulting from a variety of pathological insults (Gelbard et al, 1993;Chao and Hu, 1994;Le et al, 1997;Hermann et al, 2001). …”

Section: Introductionmentioning

confidence: 99%

Differential Regulation of AMPA Receptor and GABA Receptor Trafficking by Tumor Necrosis Factor-α

Stellwagen¹,

Beattie²,

Seo³

et al. 2005

J. Neurosci.

867

731

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The proinflammatory cytokine tumor necrosis factor-␣ (TNF␣) causes a rapid exocytosis of AMPA receptors in hippocampal pyramidal cells and is constitutively required for the maintenance of normal surface expression of AMPA receptors. Here we demonstrate that TNF␣ acts on neuronal TNFR1 receptors to preferentially exocytose glutamate receptor 2-lacking AMPA receptors through a phosphatidylinositol 3 kinase-dependent process. This increases excitatory synaptic strength while changing the molecular stoichiometry of synaptic AMPA receptors. Conversely, TNF␣ causes an endocytosis of GABA A receptors, resulting in fewer surface GABA A receptors and a decrease in inhibitory synaptic strength. These results suggest that TNF␣ can regulate neuronal circuit homeostasis in a manner that may exacerbate excitotoxic damage resulting from neuronal insults.

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“…AMPAR blockade is also neuroprotective in preventing cell death due to Parkinsonism and seizures (26,33). Perhaps the most compelling evidence for a role of ␣-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) in ECD is that transgenic mice expressing high levels of AMPARs are more susceptible to focal ischemia than wild-type mice (28). Despite this evidence, research into the role of AMPARs in anoxia tolerance has been overlooked, despite extensive research into NMDAR-mediated cell death.…”

mentioning

confidence: 99%

AMPA receptors undergo channel arrest in the anoxic turtle cortex

Pamenter¹,

Shin²,

Buck³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Without oxygen, all mammals suffer neuronal injury and excitotoxic cell death mediated by overactivation of the glutamatergic N-methyl-D-aspartate receptor (NMDAR). The western painted turtle can survive anoxia for months, and downregulation of NMDAR activity is thought to be neuroprotective during anoxia. NMDAR activity is related to the activity of another glutamate receptor, the ␣-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR). AMPAR blockade is neuroprotective against anoxic insult in mammals, but the role of AMPARs in the turtle's anoxia tolerance has not been investigated. To determine whether AMPAR activity changes during hypoxia or anoxia in the turtle cortex, whole cell AMPAR currents, AMPAR-mediated excitatory postsynaptic potentials (EPSPs), and excitatory postsynaptic currents (EPSCs) were measured. The effect of AMPAR blockade on normoxic and anoxic NMDAR currents was also examined. During 60 min of normoxia, evoked peak AMPAR currents and the frequencies and amplitudes of EPSPs and EPSCs did not change. During anoxic perfusion, evoked AMPAR peak currents decreased 59.2 Ϯ 5.5 and 60.2 Ϯ 3.5% at 20 and 40 min, respectively. EPSP frequency (EPSP ƒ) and amplitude decreased 28.7 Ϯ 6.4% and 13.2 Ϯ 1.7%, respectively, and EPSCƒ and amplitude decreased 50.7 Ϯ 5.1% and 51.3 Ϯ 4.7%, respectively. In contrast, hypoxic (PO2 ϭ 5%) AMPAR peak currents were potentiated 56.6 Ϯ 20.5 and 54.6 Ϯ 15.8% at 20 and 40 min, respectively. All changes were reversed by reoxygenation. AMPAR currents and EPSPs were abolished by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). In neurons pretreated with CNQX, anoxic NMDAR currents were reversibly depressed by 49.8 Ϯ 7.9%. These data suggest that AMPARs may undergo channel arrest in the anoxic turtle cortex.N-methyl-D-aspartate receptor; excitotoxic cell death; spike arrest THE WESTERN PAINTED TURTLE (Chrysemys picta belli) can survive without oxygen for days to months (43). This tolerance is predicated on the turtle's ability to maintain neuronal function by using anaerobically produced ATP. In contrast, mammals cannot survive on anaerobic metabolism alone. Oxygen deprivation induces elevations in excitatory amino acids, which leads to overexcitation of glutamate receptors, ATP loss, anoxic depolarization, excessive Ca 2ϩ influx, and rapid excitotoxic cell death (ECD) (6,11,24,36,41). Two glutamate receptors, the N-methyl-D-aspartate receptor (NMDAR) and the ␣-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR), are the principle mediators of ECD. In mammals, the activity of both receptors is increased during hypoxia (14, 29), and blockade of either receptor is neuroprotective against global or focal ischemia (15,42).A proposed mechanism used by facultative anaerobes to prolong anoxia tolerance and prevent ECD is a decrease in membrane permeability and downregulation of ion channel or receptor activity termed "channel arrest" (17). Indeed, in contrast to the commonly observed anoxic potentiation of mammalian NMDAR currents, turtle NMDARs underg...

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Enhanced neuronal death from focal ischemia in AMPA-receptor transgenic mice

Cited by 32 publications

References 21 publications

Differential localization of the GluR1 and GluR2 subunits of the AMPA-type glutamate receptor among striatal neuron types in rats

Differential localization of the GluR1 and GluR2 subunits of the AMPA-type glutamate receptor among striatal neuron types in rats

Differential Regulation of AMPA Receptor and GABA Receptor Trafficking by Tumor Necrosis Factor-α

AMPA receptors undergo channel arrest in the anoxic turtle cortex

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