6-cyano-7-nitroquinoxaline-2-3-dione has been researched along with Stroke* in 3 studies
3 other study(ies) available for 6-cyano-7-nitroquinoxaline-2-3-dione and Stroke
| Article | Year |
|---|---|
Neuroprotection against supra-lethal 'stroke in a dish' insults by an anti-excitotoxic receptor antagonist cocktail.
The goal of this study was to identify cocktails of drugs able to protect cultured rodent cortical neurons against increasing durations of oxygen-glucose deprivation (OGD). As expected, a cocktail composed of an NMDA and AMPA receptor antagonists and a voltage gated Ca Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; Dizocilpine Maleate; Glucose; Humans; Neuroprotection; Neuroprotective Agents; Nifedipine; Oxygen; Protein Serine-Threonine Kinases; Receptors, AMPA; Receptors, N-Methyl-D-Aspartate; Stroke; TRPM Cation Channels | 2022 |
Neuronal circuit remodeling in the contralateral cortical hemisphere during functional recovery from cerebral infarction.
Recent advances in functional imaging of human brain activity in stroke patients, e.g., functional magnetic resonance imaging, have revealed that cortical hemisphere contralateral to the infarction plays an important role in the recovery process. However, underlying mechanisms occurring in contralateral hemisphere during functional recovery have not been elucidated. We experimentally induced a complete infarction of somatosensory cortex in right hemisphere of mice and examined the neuronal changes in contralateral (left) somatosensory cortex during recovery. Both basal and ipsilateral somatosensory stimuli-evoked neuronal activity in left (intact) hemisphere transiently increased 2 d after stroke, followed by an increase in the turnover rate of usually stable mushroom-type synaptic spines at 1 week, observed by using two-photon imaging in vivo. At 4 weeks after stroke, when functional recovery had occurred, a new pattern of electrical circuit activity in response to somatosensory stimuli was established in intact ipsilateral hemisphere. Thus, the left somatosensory cortex can compensate for the loss of the right somatosensory cortex by remodeling neuronal circuits and establishing new sensory processing. This finding could contribute to establish the effective clinical treatments targeted on the intact hemisphere for the recovery of impaired functions and to achieve better quality of life of patients. Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; Action Potentials; Animals; Brain Infarction; Dendritic Spines; Excitatory Amino Acid Antagonists; Functional Laterality; Luminescent Proteins; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Neuronal Plasticity; Neurons; Physical Stimulation; Recovery of Function; Somatosensory Cortex; Stroke; Synapses; Time Factors | 2009 |
Activation of a novel injury-induced calcium-permeable channel that plays a key role in causing extended neuronal depolarization and initiating neuronal death in excitotoxic neuronal injury.
Protracted elevation in intracellular calcium caused by the activation of the N-methyl-d-aspartate receptor is the main cause of glutamate excitotoxic injury in stroke. However, upon excitotoxic injury, despite the presence of calcium entry antagonists, calcium unexpectedly continues to enter the neuron, causing extended neuronal depolarization and culminating in neuronal death. This phenomenon is known as the calcium paradox of neuronal death in stroke, and it represents a major problem in developing effective therapies for the treatment of stroke. To investigate this calcium paradox and to determine the source of this unexpected calcium entry after neuronal injury, we evaluated whether glutamate excitotoxicity activates an injury-induced calcium-permeable channel responsible for conducting a calcium current that underlies neuronal death. We used a combination of whole-cell and single-channel patch-clamp recordings, fluorescent calcium imaging, and neuronal cell death assays in a well characterized primary hippocampal neuronal culture model of glutamate excitotoxicity/stroke. Here, we report activation of a novel calcium-permeable channel upon excitotoxic glutamate injury that carries calcium current even in the presence of calcium entry inhibitors. Blocking this injury-induced calcium-permeable channel for a significant time period after the initial injury is still effective in preventing calcium entry, extended neuronal depolarization, and delayed neuronal death, thereby accounting for the calcium paradox. This injury-induced calcium-permeable channel represents a major source for the initial calcium entry following stroke, and it offers a new target for extending the therapeutic window for preventing neuronal death after the initial excitotoxic (stroke) injury. Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; Animals; Animals, Newborn; Apoptosis; Calcium; Calcium Channel Blockers; Calcium Channels; Cells, Cultured; Chlorides; Cobalt; Dizocilpine Maleate; Dose-Response Relationship, Drug; Electric Impedance; Ethosuximide; Gadolinium; Glutamic Acid; Membrane Potentials; Neurons; Nifedipine; omega-Conotoxins; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Sodium; Stroke; Zinc Compounds | 2007 |