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Possible Anti-ApoptoticActivity of Carnitines on Excitatory Amino Acid-Induced Neurotoxicity

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Carnitine Today

Abstract

Glutamate is the primary excitatory neurotransmitter in the brain. At the neuronal synapse, it interacts with a variety of receptors that specify neurotransmitter interactions and transmit information into target cells. The vast majority of synapses in the central nervous system use glutamate as a neurotransmitter to produce rapid neuronal excitation.1,2 Glutamate neurotransmission also participates in neuronal plasticity and neurotoxicity Neuronal plasticity elicited by glutamate is exemplified by long-term potentiation (LTP) in the hippocampus3 and long term depression in the cerebellum.4 However, at supraphysiological concentrations, it is a potent excitotoxin that causes neuronal death through a cascade of cationic and second messenger events.5,6 In fact, in many neurologic disorders, injury to neurons may be partly caused by overstimulation of receptors for excitatory amino acids, including glutamate and aspartate. These neurologic conditions range from acute insults such as stroke, hypoglycemia and epilepsy to chronic neurodegenerative diseases such as Hungtington’s disease, AIDS- dementia complex, amyotrophic lateral sclerosis, and perhaps Alzheimer’s disease. Furthermore, a plethora of unrelated molecules including HIV gpl2O, HIV-Tat, tumor necrosis factor (TNF)-a, platelet-activating factor (PAF), interleukin-6 (IL-6), arachidonic acid metabolites, reactive oxygen species and nitric oxide (NO)7–15 can trigger neuronal cell death by converging their actions into a common pathway that involves ionotropic glutamate receptors (glutamate-activated ion channels that regulate intracellular Ca2+).

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Alesse, E., Cifone, G., Angelucci, A., Zazzeroni, F., De Simone, C. (1997). Possible Anti-ApoptoticActivity of Carnitines on Excitatory Amino Acid-Induced Neurotoxicity. In: Carnitine Today. Molecular Biology Intelligence Unit. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-6005-0_13

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  • DOI: https://doi.org/10.1007/978-1-4615-6005-0_13

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-0-412-13271-1

  • Online ISBN: 978-1-4615-6005-0

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