Excitotoxicity on Cultured Cortical Neurons
This meeting is focused on two important properties of neurotransmitter glutamate. First, glutamate can regulate the long-term behavior of at least some of the excitatory synapses where it serves as neurotransmitter. This regulation provides a means for dynamic synaptic plasticity and may play a key role in normal functions such as memory and learning. Second, excess exposure to glutamate can destroy neurons, a process Olney (1986) called “excitotoxicity.” Excitotoxicity may contribute to pathogenesis of certain acute or chronic neurological diseases. While glutamate-mediated synaptic regulation and glutamate-mediated neuronal death occur in different settings, a theme of the present meeting is that the two processes may overlap substantially at the level of underlying mechanism.
KeywordsToxicity Superoxide Glycine Choline Ketamine
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- Baimbridge KG, Kao J (1988) Calbindin D-28K protects against glutamate-induced neurotoxicity in rat CA1 pyramidal neuron cultures. Soc Neurosci Abstr 14:1264.Google Scholar
- Garthwaite J (1985) Cellular uptake disguises action of L-glutamate on N-methyl-D-aspartate receptors. With an appendix: diffusion of transported amino acids into brain slices. Br J Pharmacol 85:297–307.Google Scholar
- Kurth MC, Weiss JH, Choi DW (1989) Relationship between glutamate-induced 45Ca influx and resultant neuronal injury in cultured cortical neurons. Neurology 39:217.Google Scholar
- Lipton SA, Kater SB (1989) Neurotransmitter regulation of neuronal outgrowth. plasticity and survival, trends Neurosci 12:265–270.Google Scholar
- Marcoux FW, Goodrich JE, Probert AW, Dominick MA (1983) Ketamine prevents glutamate-induced calcium influx and ischemia nerve cell injury. In: Domino EF, Kamenka J (eds) Sigma and Phenyclidine-Like Compounds as Molecular Probes in Biology. NPP Books, Ann Arbor, Michigan, pp 735–746.Google Scholar
- Mattson MP, Guthrie PB, Hayes BC, Kater SB (1990) Roles for mitotic history in the generation and degeneration of hippocampal neuroarchitecture. J Neurosci 9:1223–1232.Google Scholar
- Mody I, MacDonald JF, Baimbridge KG (1988) Release of intracellular calcium following activation of excitatory amino acid receptors in cultured hippocampal neurons. Soc Neurosci Abstr 14:94.Google Scholar
- Monyer H, Hartley DM, Ehsani H, Seeburg PH, Choi DW (1990) Muscimol attenuates slow excitatory amino acid-induced injury of cultured cortical neurons. Soc Neurosci Abst, in press.Google Scholar
- Morad M, Dichter M, Tang CM (1988) The NMDA activated current in hippocampal neurons is highly sensitive to [H+]. Soc Neurosci Abstr 14:791.Google Scholar
- Nachsen DA, Sanchez-Armass S, Weinstein Am (1986) The regulation of cytosolic calcium in rat brain synaptosomes by sodium-dependent calcium efflux. J Physiol 381:17–28.Google Scholar
- Siesjo BK, Rehncrona S, Smith D (1980) Neuronal cell damage in the brain: possible involvement of oxidative mechanisms. Acta Physiol Scand [Suppl] 492:121–128.Google Scholar