Naural Responses to Injury: Prevention, Protection, and Repair. Revised. Volume 4. Neurochemical Protection of the Brain, Neural Plasticity and Repair.
Abstract
Traumatic brain injury is characterized by multiple phases of damage; including primary tissue damage and bleeding at the site of impact; secondary damage, including brain edema, ischemia, the diffusion of toxic substances beyond the initial site of injury and delayed neuronal death; and long-term epileptogenic changes in synaptic plasticity. A common motif at the cellular level of these various forms of neurotrauma is the over-release of neurotransmitters, the stimulation of post-synaptic receptors, and the subsequent accumulation of abnormally high concentrations of second messengers. The major neurotransmitter involved in neuronal damage is thought to be the excitatory amino acid L-glutamate. Glutamate triggers calcium entry into post-synaptic neurons via the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors (Rotlunan and Olney, 1986, 1987; Choi 1988), and so the activation of many calcium-dependent signaling pathways. The major focus of research in our laboratory has been the activation of calcium- dependent phospholipases A2, the release from membrane phospholipids of bioactive lipids, including free arachidonic acid (AA) and platelet-activating factor (PAF), and the signaling pathways then activated. We and other groups have shown the neuroprotective properties of pharmacological agents targeting bioactive lipid signaling cascades. Detailed characterization of these processes, and the downstream events that link the over-accumulation of bioactive lipids to long-term changes in brain physiology, is important in identifying the best therapeutic targets for the treatment of traumatic brain injury.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 1997
- Accession Number
- ADA353806
Entities
People
- Nicolas G Bazan
Organizations
- Louisiana State University