Research reportThe effect of NMDA, AMPA/kainate, and calcium channel antagonists on traumatic cortical neuronal injury in culture
References (37)
- et al.
6,7-Dinitro quinoxaline-2,3-dion and 6-nitro,7-cyano-quinoxaline-2,3-dion antagonise responses to NMDA in the rat spinal cord via an action at the strychnine-insensitive glycine receptor
Eur. J. Pharmacol.
(1988) Glutamate neurotoxicity and diseases of the nervous system
Neuron
(1988)- et al.
Experimental fluid percussion brain injury: vascular disruption and neuronal and glial alterations
Brain Res.
(1989) - et al.
Neurotoxicity of excitatory amino acid receptor agonists in rat cerebellar slices: dependence on calcium concentration
Neurosci. Lett.
(1986) - et al.
Antagonism of non-NMDA receptors augments the neuroprotective effect of NMDA receptor blockade in cortical cultures subjected to prolonged deprivation of oxygen and glucose
Brain Res.
(1991) - et al.
Quantitative determination of glutamate mediated cortical neuronal injury in cell culture by lactate dehydrogenase efflux assay
J. Neurosci. Methods
(1987) - et al.
Selective blockade of non-NMDA receptors does not block rapidly triggered glutamate-induced neuronal death
Brain Res.
(1991) - et al.
Excitotoxicity and the NMDA receptor
Trends Neurosci.
(1987) - et al.
Delayed neurotoxicity of excitatory amino acids in vitro
Neuroscience
(1987) - et al.
Traumatic neuronal injury in vitro is attenuated by NMDA antagonists
Neuron
(1989)
Effects of felopidine (a dihydropyridine calcium channel blocker) and analogues on calmodulin-dependent enzymes
Biochem. Pharmacol.
Potassium and calcium changes in injured spinal cords
Brain Res.
Widening potential for Ca2+ antagonists: non-L-type Ca2+ channel interaction
Trends Pharm. Sci.
Cerebral pressure following trauma
Am. J. Physiol.
Effect of Ca2+ channel blockers on Ca2+ translocation across synaptosomal membranes
J. Neurochem.
Ionic dependence of glutamate neurotoxicity in cortical cell culture
J. Neurosci.
Methods for antagonizing glutamate neurotoxicity
Cerebrovasv. Brain Metab. Rev.
Glutamate neurotoxicity in cortical cell culture
J. Neurosci.
Cited by (96)
A new in vitro injury model of mouse neurons induced by mechanical scratching
2012, Neuroscience LettersIron accumulation and neurotoxicity in cortical cultures treated with holotransferrin
2011, Free Radical Biology and MedicinePost-injury treatment with lipopolysaccharide or lipooligosaccharide protects rat neuronal and glial cell cultures
2011, Brain Research BulletinCitation Excerpt :In vitro models can reproduce sequelae of human CNS injuries such as changes in cellular ultrastructure, free radical generation, and ionic homeostasis. The scratch model of injury that we used is thought to most closely mimic a penetrating TBI which can be caused by wounds such as from a gunshot, shrapnel, or a motor vehicle crash [12,38,45,46]. Other types of in vitro models of TBI include injury of cell cultures by a punch device or laser transection, and neuronal and axonal deformation models.
Apotransferrin protects cortical neurons from hemoglobin toxicity
2011, NeuropharmacologyNeural mechanobiology and neuronal vulnerability to traumatic loading
2010, Journal of BiomechanicsCitation Excerpt :Two-dimensional (2-D) or “monolayer” neuronal culturing, where the cells are attached to a planar substrate, is the simplest arrangement in which a neural network can be maintained. 2-D in vitro models of neural trauma include penetrating and blunt impact injury paradigms (Balentine et al., 1988; Regan and Choi, 1994) as well as inertial injury models (Ellis et al., 1995; Cargill and Thibault, 1996; LaPlaca and Thibault, 1997). It is critical to develop cellular systems that mimic their in vivo environment as closely as possible.
Neuroprotective effects of bone morphogenetic protein 7 (BMP7) treatment after spinal cord injury
2009, Neuroscience Letters