Anticonvulsant effect of reduced NMDA receptor expression in audiogenic DBA/2 mice

Chapman, A. Chaston; Woodburn, V.L.; Woodruff, G.N.; Bs, Meldrum

doi:10.1016/s0920-1211(96)00036-8

Cited by 23 publications

(11 citation statements)

References 45 publications

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“…* PϽ0.05; ** PϽ0.01 versus wild type group; # PϽ0.01 versus AP-5ϩglutamate; ϩ PϽ0.05 versus NBQXϩglutamate group by one-way ANOVA for repeated measures followed by Fisher's PLSD test. (Chapman et al, 1996;Zapata et al, 1997;Balosso et al, 2005) and other mechanisms should be considered. In particular, recent evidence demonstrates a significant role of astrocytic glutamate release in determining the strength of ictal events (Fellin et al, 2006), and this release is apparently reduced in p55 Ϫ/Ϫ mice (see above).…”

Section: Discussionmentioning

confidence: 99%

Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus: Implications for seizure susceptibility

et al. 2009

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Abstract-Tumor necrosis factor (TNF)-alpha is a proinflammatory cytokine acting on two distinct receptor subtypes, namely p55 and p75 receptors. TNF-alpha p55 and p75 receptor knockout mice were previously shown to display a decreased or enhanced susceptibility to seizures, respectively, suggesting intrinsic modifications in neuronal excitability. We investigated whether alterations in glutamate system function occur in these naive knockout mice with perturbed cytokine signaling that could explain their different propensity to develop seizures. Using Western blot analysis of hippocampal homogenates, we found that p55 ؊/؊ mice have decreased levels of membrane GluR3 and NR1 glutamate receptor subunits while GluR1, GluR2, GluR6/7 and NR2A/B were unchanged as compared to wild-type mice. In p75 ؊/؊ mice, GluR2, GluR3, GluR6/7 and NR2A/B glutamate receptor subunits were increased in the hippocampus while GluR1 and NR1 did not change. Extracellular single-cell recordings of the electrical activity of hippocampal neurons were carried out in anesthetized mice by standard electrophysiological techniques. Microiontophoretic application of glutamate increased the basal firing rate of hippocampal neurons in p75 ؊/؊ mice versus wild-type mice, and this effect was blocked by 2-amino-5-phosphopentanoic acid and 6-nitro-7-sulfamoyl-benzo(f)quinoxaline-2,3-dione denoting the involvement of N-methyl-D-aspartic acid and AMPA receptors. In p55؊/؊ mice, hippocampal neurons responses to glutamate were similar to wild-type mice. Spontaneous glutamate release measured by in vivo hippocampal microdialysis was significantly decreased only in p55 ؊/؊ mice. No changes were observed in KCl-induced glutamate release in both receptor knockout mice strains versus wild-type mice. These findings highlight specific molecular and functional interactions between p55 and p75 receptor-mediated signaling and the glutamate system. These interactions may be relevant for controlling neuronal excitability in physiological and pathological conditions.

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Section: Discussionmentioning

confidence: 99%

Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus: Implications for seizure susceptibility

et al. 2009

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“…Alternatively, gating impairments in DBA/2J mice might be based on alterations in glutamatergic transmission. Alterations in NMDA receptor signaling have been proposed in DBA/2J mice (Chapman et al 1996). In particular, the fact that DBA/2J mice respond to doses of NMDA antagonists ineffective in C57BL/6J mice (Lu and Wehner 1997) may suggest that NMDA receptors in DBA/2J mice might be hypofunctional.…”

Section: Discussionmentioning

confidence: 99%

Activation of GABAB receptors reverses spontaneous gating deficits in juvenile DBA/2J mice

et al. 2007

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“…A complete suppression of sound-induced seizures has been obtained by intracerebroventricular administration of antisense probe for NMDA-receptor (NR1 subunit), demonstrating the importance of NMDA receptors in this model of reflex epilepsy [42]. A very great contribution to the discovery and development of possible anticonvulsant compounds acting as antagonists of excitatory amino acid neurotransmission was obtained at Brian Meldrum's laboratory in London.…”

Section: Dba/2 Mice and Antagonists Of Excitatory Amino Acid Neurotramentioning

confidence: 99%

“…Abnormalities in the excitatory neurotransmitter system have been found in DBA/2 mice [41,42]. It has been demonstrated that excitatory amino acid antagonists of both ionotropic (NMDA and AMPA/kainate) [43][44][45][46][47] and metabotropic glutamate receptors prevent soundinduced seizures [25,48].…”

Section: Dba/2 Mice and Antagonists Of Excitatory Amino Acid Neurotramentioning

confidence: 99%

Genetically epilepsy-prone rats (GEPRs) and DBA/2 mice: Two animal models of audiogenic reflex epilepsy for the evaluation of new generation AEDs

Sarro¹,

Russo²,

Citraro³

et al. 2017

Epilepsy & Behavior

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Anticonvulsant effect of reduced NMDA receptor expression in audiogenic DBA/2 mice

Cited by 23 publications

References 45 publications

Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus: Implications for seizure susceptibility

Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus: Implications for seizure susceptibility

Activation of GABAB receptors reverses spontaneous gating deficits in juvenile DBA/2J mice

Genetically epilepsy-prone rats (GEPRs) and DBA/2 mice: Two animal models of audiogenic reflex epilepsy for the evaluation of new generation AEDs

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