Dextromethorphan protects against cerebral infarction in a rat model of hypoxia-ischemia
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Cited by (84)
The common antitussive agent dextromethorphan protects against hyperoxia-induced cell death in established in vivo and in vitro models of neonatal brain injury
2014, NeuroscienceCitation Excerpt :As relative hyperoxia cannot be prevented and therapeutic use of oxygen is often necessary in the clinical setting, the pre-clinical evaluation of substances with the potential to counteract detrimental oxygen effects is of utmost importance. DM is a common antitussive agent with multiple mechanisms of action and known anti-oxidative properties that has already proven its neuroprotective potential in several animal models of neonatal brain injury (Prince and Feeser, 1988; Laroia et al., 1997; Keller et al., 2008). To the best of our knowledge we are the first to show beneficial effects of DM in both in vitro and in vivo models of hyperoxia-induced injury in the developing brain, while ruling out a major negative impact on healthy brain tissue.
Dextromethorphan inhibits the glutamatergic synaptic transmission in the nucleus tractus solitarius of Guinea pigs
2011, Journal of Pharmacological SciencesTherapeutic use of dextromethorphan: Key learnings from treatment of pseudobulbar affect
2007, Journal of the Neurological SciencesNeuroprotective effects of hibernation-regulating substances against low-temperature-induced cell death in cultured hamster hippocampal neurons
2006, Brain ResearchCitation Excerpt :ADO acts as a neuromodulator in the CNS and the neuroprotective effect of ADO against ischemic or traumatic neuronal injury has been well documented experimentally (Gidday et al., 1995; Schubert et al., 1997; Sweeney, 1997; von Lubitz and Marangos, 1990). Moreover, opioid receptor agonists elicit neuroprotective effects against neurodegeneration induced by ischemia and trauma (Chen et al., 2005; Lyeth et al., 1995; Prince and Feeser, 1988). In this study, we investigated if hibernation-regulating substances (HRS) such as ADO, opioids and TRH would protect hippocampal cultures from low-temperature-induced neuronal cell death (LTCD).
Dextromethorphan attenuates morphine withdrawal syndrome in neonatal rats passively exposed to morphine
2002, European Journal of PharmacologyCitation Excerpt :This potency of dextromethorphan is generally close to that in suppressing morphine withdrawal syndrome in adult rats reported by others (Farzin, 1999; Mao et al., 1996). It is also within the potency range for attenuating other neuropathologies related to overactivation of the NMDA receptor in neonatal rats (Laroia et al., 1997; Prince and Feeser, 1988). In addition, the potency of MK-801 seems to be at least 40-fold higher than that of dextromethorphan, since postnatal injection of 0.5 mg/kg MK801 was as effective as that of 20 mg/kg of dextromethorphan, and prenatal co-injection of 0.1 mg/kg MK-801 was as effective as that of 10 mg/kg of dextromethorphan.
Imaging and preventing spreading depression independent of cerebral blood flow
2002, International Congress Series