By P. H. Seeburg, R. Brusa, M. Higuchi, R. Sprengel (auth.), P. H. Seeburg, I. Bresink, L. Turski (eds.)
Ernst Schering examine origin Workshop 23Excitatory Amino Acids: From Genes to Therapy Editors: P. Seeburg, I. Bresink, L. Turski during this booklet rising questions of present glutamate learn are addressed and new pathways which glutamate study may possibly soak up the long run mentioned. in view that glutamate antagonists are nonetheless the key desire for the remedy of neurodegenerative issues in people, examine actions committed in the direction of the advance of such novel medicines are the focal point of public recognition. The ebook reviews at the newest discoveries within the box of neuroprotection and neurodegeneration.
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Additional info for Excitatory Amino Acids: From Genes to Therapy
Example text
4 Conclusions .......................................... " References ................................................. 1 Introduction Glutamate receptors (GluRs) mediate normal excitatory neurotransmission and playa critical role in a number of other important physiological functions such as synaptogenesis, formation of neuronal circuitry, and synaptic plasticity, including long-term potentiation and long-term depression. E. Pellegrini-Giampietro cluding ischemia, trauma, hypoglycemia, and epileptic seizures.
LA; G) (Lomeli et al. 1994). Editing at the RIG site is specific for GluR2, -3, and -4, and is about 80%-90% complete in adult rat brain (Fig. lA). Immediately adjacent to the RIG site, one of two cassettes named flip and flop (Sommer et al. 1990), each containing 38 amino acids, is ..... Fig. lA-C. Proposed secondary structure of GluR subunits depicting critical sites conferring functional diversity on a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. A A GluR subunit in its linear sequence and inserted into the cell membrane.
Neuronal mitochondria are ideally equipped to cooperate with Ca in the sensing and integrating of many aspects of cellular activity and then coordinating the appropriate response to these events. This is certainly true with respect to both necrotic and apoptotic aspects of excitotoxic neurodegeneration. For example, mitochondrial Ca uptake can trigger the production of superoxide (02-) and other free radicals that may be important mediators of both short and long-term neuronal events (Fig. 2) (Bindokas et al.
