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The role of group I metabotropic glutamate receptors in neuronal excitotoxicity in Alzheimer s disease Tsai VW; Scott HL; Lewis RJ; Dodd PRNeurotox Res 2005[]; 7 (1-2): 125-41Neurodegenerative diseases such as Huntington's disease, ischemia, and Alzheimer's disease (AD) are major causes of death. Recently, metabotropic glutamate receptors (mGluRs), a group of seven-transmembrane-domain proteins that couple to G-proteins, have become of interest for studies of pathogenesis. Group I mGluRs control the levels of second messengers such as inositol 1,4,5-triphosphate (IP3), Ca2+ ions and cAMP. They elicit the release of arachidonic acid via intracellular Ca2+ mobilization from intracellular stores such as mitochondria and endoplasmic reticulum. This facilitates the release of glutamate and could trigger the formation of neurofibrillary tangles, a pathological hallmark of AD. mGluRs regulate neuronal injury and survival, possibly through a series of downstream protein kinase and cysteine protease signaling pathways that affect mitochondrially mediated programmed cell death. They may also play a role in glutamate-induced neuronal death by facilitating Ca(II) mobilization. Hence, mGluRs have become a target for neuroprotective drug development. They represent a pharmacological path to a relatively subtle amelioration of neurotoxicity because they serve a modulatory rather than a direct role in excitatory glutamatergic transmission.|Alzheimer Disease/*metabolism[MESH]|Animals[MESH]|Excitatory Amino Acid Agents/metabolism/*toxicity[MESH]|Humans[MESH]|Neurons/drug effects/*pathology[MESH]|Receptors, Metabotropic Glutamate/agonists/antagonists & inhibitors/*physiology[MESH] |
