ucn-1028-c and Brain-Injuries

Activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors is implicated in the pathophysiology of traumatic brain injury. Here, the effects of mechanical injury on the voltage-dependent magnesium (Mg2+) block of NMDA currents in cultured rat cortical neurons were examined. Stretch-induced injury was found to reduce the Mg2+ blockade, resulting in significantly larger ionic currents and increases in intracellular free calcium (Ca2+) concentration after NMDA stimulation of injured neurons. The Mg2+ blockade was partially restored by increased extracellular Mg2+ concentration or by pretreatment with the protein kinase C inhibitor calphostin C. These findings could account for the secondary pathological changes associated with traumatic brain injury.

Topics: Animals; Brain Injuries; Calcium; Cells, Cultured; Cerebral Cortex; Dizocilpine Maleate; Enzyme Inhibitors; Excitatory Amino Acid Antagonists; Magnesium; Membrane Potentials; N-Methylaspartate; Naphthalenes; Neurons; Patch-Clamp Techniques; Protein Kinase C; Rats; Receptors, N-Methyl-D-Aspartate