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L-glutamate is the major excitatory neurotransmitter in the central nervous system (CNS). It contribute in various physiological conditions such as brain development, synaptic plasticity, memory and learning. However, increasing of the extracellular glutamate concentration and overactivation of glutamate receptors in particular ionotropic subtypes leads to excitotoxicity which is the fundamental pathological pathway of neuronal injury. Due to lack of extracellular enzymatic destruction, the removal of released glutamate is achieved through the excitatory amino acid transporters (EAATs) which are distributed in glia that tightly surround the synaptic clefts, as well as in neurons. EAATs which known as Na+-dependent high-affinity glutamate transporters are the main responsible for maintaining extracellular glutamate concentration below excitotoxic levels. Moreover another membrane transporters regulating the flux of glutamate in different areas of the CNS. This system is cystine-glutamate exchanger (XCG-) that is Na+-independent system. Dysfunction of EAATs has been implicated in both acute insults e.g. stroke, trauma and chronic neurological and neuropsychiatric disorders e.g. amyotrophic lateral sclerosis, epilepsy, schizophrenia and Alzheimer's disease. Therefore, the purpose of this review article is to explain the pathway of glutamate biosynthesis, its release into CNS, discribing and elaborating Glutamate transporters, activites and their role in excitoxcity in CNS.

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Background and Objective: Monosodium glutamate (MSG) is used as a food additive. Several studies have reported the adverse effects of Monosodium glutamate on the testis and brain. This study was performed to determine the effect of Monosodium glutamate in rat cerebellum. Methods: In this experimental study, 24 adult wistar rats randomly allocated into three groups including experiment A, experiment B and control (C). The animals in experiment A and B were received 3g and 6g of MSG thoroughly mixed with their feeds for 14 days, respectively. Animals in control group were received MSG free diet. Food and water for rats to be free in all of experimental time. The rats were sacrificed on fifteen day. The cerebellum dissected and fixed with formalin 10% buffer and stained with hematoxylin and eosin. Results: Disorders and detachment were observed in Purkinje and granular cell layers. Neural cell distribution in granular layer redeuced in the experimental groups. Cellular degenerative changes in the granular layer of the experimental B were more severe than experimental group A. The mean number of neuron of the granular layer in the experimental A, B and control groups were 2750, 2140 and 3150, respectively. Conclusion: The consumption of monosodium glutamate dose dependly causes histopathological changes and reduces the number of the cerebellumllar neurons in adult rat.