IndraLab

Statements



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"NMDA preconditioning and neuroprotection in vivo : Delayed onset of kainic acid induced neurodegeneration and c-Fos attenuation in CA3a neurons."

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"In addition, NMDA antagonists can block the c-fos activation observed in several brain regions during morphine withdrawal (e.g."

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"The non competitive N-methyl-D-aspartate antagonists ketamine (100 mg/kg, i.p.) and MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a, d] cyclohepten-5,10-imine maleate] (1 and 3 mg/kg, i.p.) markedly reduced c-fos activation."

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"Like the competitive antagonists, intrastriatal infusion of the non competitive NMDA antagonist MK-801 partially decreased c-fos, but not zif268, mRNA in the area around the microdialysis probe."

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"The N-methyl-D-aspartate (NMDA) antagonist, MK-801 (4 mg/kg, i.p.) inhibited c-fos and junB mRNA induction in the cortex, striatum, thalamus, and hippocampus but not in the substantia nigra."

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"The N-methyl-D-aspartate (NMDA) antagonist, MK-801 (4 mg/kg, i.p.) inhibited c-fos and junB mRNA induction in the cortex, striatum, thalamus, and hippocampus but not in the substantia nigra."

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"NMDA-stimulated c-Fos protein induction was markedly suppressed by EGTA ( p < 0.001, Fig. 5 A), suggesting the involvement of calcium ion influx through NMDA receptor."

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"In addition, there is an increased release of glutamate in several brain regions during morphine withdrawal (e.g., nucleus accumbens, spinal cord) and NMDA antagonists can block c-fos activation in se[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"NMDA preconditioning and neuroprotection in vivo : delayed onset of kainic acid induced neurodegeneration and c-Fos attenuation in CA3a neurons."