Dextromethorphan protects against cerebral injury following transient, but not permanent, focal ischemia in rats
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Animal models of cerebral ischemia: A review
2020, Biomedicine and PharmacotherapyContrasting roles of immune cells in tissue injury and repair in stroke: The dark and bright side of immunity in the brain
2017, Neurochemistry InternationalCitation Excerpt :It will also affect similar regions of the brain, including both the cortex and striatum. However, the lack of reperfusion will consequently limit the chance of hemorrhage and result in central nervous system (CNS) resident microglia playing a more prominent role in stroke pathology (Britton et al., 1997; Kostulas et al., 2002; Li and Stephenson, 2002; Zhang et al., 1995; Burggraf et al., 2005; Lo, 2008a). Recently, methods have been developed that limit the amount of time it takes to induce stroke in mice while simultaneously reducing the variability in infarct location and volume.
Dextromethorphan: An update on its utility for neurological and neuropsychiatric disorders
2016, Pharmacology and TherapeuticsCitation Excerpt :In this study, the authors also reported that nifedipine (an L-type VGCC blocker) prevented ERK5 activation to a similar extent as DM, suggesting that DM may in part inhibit VGCCs to regulate ERK5 activity (Wang et al., 2004). Interestingly, in a rat model of transient, focal cerebral ischemia, DM attenuated the injury-related increase in rectal temperature, which was associated with its ability to protect neurons in temperature regulating hypothalamic centers (Britton et al., 1997). A strong correlation between rat rectal and brain temperatures has been shown during focal ischemic insults (Zhang et al., 1993), suggesting that DM may improve outcome in certain ischemic cases by limiting the transient increase in body temperature (Britton et al., 1997).
Low dose dextromethorphan attenuates moderate experimental autoimmune encephalomyelitis by inhibiting NOX2 and reducing peripheral immune cells infiltration in the spinal cord
2011, Neurobiology of DiseaseCitation Excerpt :Lacking the affinity to opioid receptors, DM works as a non-competitive antagonist of NMDA receptors, inhibits voltage gated Ca2+-channels, and stimulates sigma-1 receptors at relatively high doses (Werling et al., 2007). Due to these properties, DM has been shown to be neuroprotective in models of cerebral ischemia, spinal cord injury, epilepsy and Parkinson's disease (Britton et al., 1997; Kim et al., 1996; Steinberg et al., 1988; Topsakal et al., 2002; Zhang et al., 2004). At lower doses, DM or other morphinans are known to inhibit NOX2 mediated production of ROS in activated microglia/macrophages by the reduction of p47phox translocation to the cell membrane through the inhibition of ERK 1/2 phosphorylation (Liu et al., 2009; Qian et al., 2007).
Neuropsychotoxic and neuroprotective potentials of dextromethorphan and its analogs
2011, Journal of Pharmacological Sciences