Neuropharmacology and analgesiaMarked diversity in the action of growth factors on N-methyl-d-rmaspartate-induced neuronal degeneration
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Cited by (35)
Is physical activity beneficial for recovery in temporal lobe epilepsy? Evidences from animal studies
2009, Neuroscience and Biobehavioral ReviewsLong-term effects of environmental stimulation following hypoxia-ischemia on the oxidative state and BDNF levels in rat hippocampus and frontal cortex
2009, Brain ResearchCitation Excerpt :In agreement with that, Koh et al. (1995) demonstrated that BDNF treatment markedly potentiates necrotic death induced by exposure to oxygen-glucose deprivation or N-methyl-d-aspartate (NMDA) in murine cortical cell cultures. Accordingly, short-term pretreatment with BDNF significantly potentiates NMDA-induced neurodegeneration (Prehn, 1996). The molecular mechanisms may be related to effects of BDNF on ion channels, since it can trigger depolarization of neurons by activating the sodium channel (Blum et al., 2002) and induces calcium release from the endoplasmic reticulum via a pathway activated by a trkB receptor (Rose et al., 2003).
Effect of a neuroprotective exercise protocol on oxidative state and BDNF levels in the rat hippocampus
2008, Brain ResearchCitation Excerpt :However, there is also evidence that BDNF may increase neuronal vulnerability to excitotoxicity. Koh et al. (1995) demonstrated that treatment with BDNF markedly potentiated necrotic death induced by exposure to oxygen–glucose deprivation or N-methyl-d-aspartate (NMDA) in murine cortical cell cultures, as well as, short-term pretreatment with BDNF significantly potentiate NMDA-induced neurodegeneration (Prehn, 1996). The molecular mechanisms may be related to the action of BDNF on ions channels, since BDNF can trigger depolarization of neurons by activating the sodium channel (Blum et al., 2002) and produce calcium release from the endoplasmic reticulum via a pathway activated by a trkB receptor (Rose et al., 2003).
Interleukin-1β regulation of N-type Ca<sup>2+</sup> channels in cortical neurons
2006, Neuroscience LettersAgmatine protects against cell damage induced by NMDA and glutamate in cultured hippocampal neurons
2006, Brain ResearchCitation Excerpt :Nevertheless, our experiments and those of Abe et al. (2003) do suggest that whether agmatine exerts neuroprotection or neurotoxicity partly depends on the experimental conditions, including the concentrations of K+ and agmatine applied. The ability of NMDA to induce apoptosis in cultured hippocampal neurons has been well documented (Diebaili et al., 2002; Vincent et al., 2002; Kajta et al., 2004; Prehn, 1996; Lee et al., 2003). Therefore, the NMDA induced neuronal death observed in the present study might also be due to apoptosis.
Transforming growth factor-β signalling in brain disorders
2006, Cytokine and Growth Factor Reviews
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