Browsing by Subject "Glutamate"

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    Evaluation of antioxidant activity and nutritional composition of flavoured dehydrated soups packaged in different formats. Reducing the sodium content
    (Springer, 2015-07-15) Martínez Tomé, Magdalena; Murcia, M. Antonia; Mariscal, Miguel; Lorenzo, Mª Luisa; Gómez Murcia, V; Bibiloni, Mar; Jiménez Monreal, Antonia M.; Tecnología de Alimentos, Nutrición y Bromatología
    The antioxidant activity and nutritional composition of four dehydrated soups (vegetables, meat, chicken and fish) packaged in four formats —carton, plastic, and aluminium bags (the last with and without modified atmosphere) — were evaluated during 12 months’ storage. The results showed that all four soups had a good or very good antioxidant capacity as tested by the lipid peroxidation, deoxyribose, and Trolox equivalent antioxidant capacity (TEAC) tests. Of interest from a nutritional point of view was the finding that the lipid fraction of all the soups was below 1 %. The sodium content of the four soups and their ingredients was also analysed. By modifying some of the ingredients, a 25%reduction in the sodium content of the soups was obtained, permitting them to be labelled as Bsodium reduced^. The monosodium glutamate (MSG) content of the reformulated soups (lower sodium content) was below levels permitted by European legislation .
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    Glutamate-like immunoreactivity in axon terminals from the olfactory bulb to the piriform cortex
    (Murcia : F. Hernández, 1998) Hennequet, L.; Gondra, J.; Sendino, J.; Ortega, F.
    A highly specific anti-glutamate monoclonal antibody, mAb2D7, was used together with light and electron microscopy to elucidate the role played by the amino acid glutamate in the projection from the olfactory bulb to the piriform cortex in the rat. By light microscopy, glutamate-like immunoreactivity was observed in neuronal cell bodies and in the neuropil of the piriform cortex. Double labelling experiments which involved injections of wheat germ agglutinin-horseradish peroxidase into the olfactory bulb and a postembedding immunogold method for electron microscopy revealed anterogradely labelled terminals making asymmetric synaptic contacts on dendrites in the piriform cortex which contained high levels of glutamate as assessed by quantification. These results further support a role for glutamate as a neurotransmitter in the efferent pathway of the rat olfactory bulb.
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    Glutamate-like immunoreactivity in axon terminals from the olfactory bulb to the piriform cortex
    (Murcia : F. Hernández, 1998) Hennequet, L.; Gondra, J.; Sendino, J.; Ortega, F.
    A highly specific anti-glutamate monoclonal antibody, mAb2D7, was used together with light and electron microscopy to elucidate the role played by the amino acid glutamate in the projection from the olfactory bulb to the piriform cortex in the rat. By light microscopy, glutamate-like immunoreactivity was observed in neuronal cell bodies and in the neuropil of the piriform cortex. Double labelling experiments which involved injections of wheat germ agglutinin-horseradish peroxidase into the olfactory bulb and a postembedding immunogold method for electron microscopy revealed anterogradely labelled terminals making asymmetric synaptic contacts on dendrites in the piriform cortex which contained high levels of glutamate as assessed by quantification. These results further support a role for glutamate as a neurotransmitter in the efferent pathway of the rat olfactory bulb.
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    Roles of glutamate in brain injuries after subarachnoid hemorrhage
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Kawakita, Fumihiro; Kanamaru, Hideki; Asada, Reona; Suzuki, Yume; Nampei, Mai; Nakajima, Hideki; Oinaka, Hiroki; Suzuki, Hidenori
    Aneurysmal subarachnoid hemorrhage (SAH) is a stroke type with a high rate of mortality and morbidity. Post-SAH brain injury as a determinant of poor outcome is classified into the following two types: early brain injury (EBI) and delayed cerebral ischemia (DCI). EBI consists of various acute brain pathophysiologies that occur within the first 72 hours of SAH in a clinical setting. The underlying mechanisms of DCI are considered to be cerebral vasospasm or microcirculatory disturbance, which develops mostly 4 to 14 days after clinical SAH. Glutamate is the principal neurotransmitter in the central nervous system, but excessive glutamate is known to induce neurotoxicity. Experimental and clinical studies have revealed that excessive glutamates are released after SAH. In addition, many studies have reported the relationships between excessive glutamate release or overactivation of glutamate receptors and excitotoxicity, cortical spreading depolarization, seizure, increased blood-brain barrier permeability, neuroinflammation, microthrombosis formation, microvasospasm, cerebral vasospasm, impairments of brain metabolic supply and demand, impaired neurovascular coupling, and so on, all of which potentially contribute to the development of EBI or DCI. As glutamates always exert their functions through one or more of 4 major receptors of glutamates, it would be valuable to know the mechanisms as to how glutamates cause these pathologies, and the possibility that a glutamate receptor antagonist may block the pathologies. To prevent the mechanistic steps leading to glutamatemediated neurotoxicity may ameliorate SAH-induced brain injuries and improve the outcomes. This review addresses the current knowledge of glutamate-mediated neurotoxicity, focusing on EBI and DCI after SAH.