Research reportEffects of maternal oral administration of monosodium glutamate at a late stage of pregnancy on developing mouse fetal brain
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2021, Toxicology ReportsCitation Excerpt :On the contrary, higher intracellular Ca2+ further enters and activates different cellular organelles (e.g., nucleus, mitochondria, endoplasmic reticulum), proteases, and caspases lead to activation of the apoptotic pathway by the consumption of MSG [9]. During pregnancy, MSG consumption induces obesity with downregulation of growth hormones, insulin-like growth factor-1 (IGF-1), reduces IntelliCage place learning and cue discrimination, impairs seizure threshold [80,81]. Moreover, uterine exposure to MSG also altered cerebral morphology and functions by up-regulation of pro-apoptotic genes and thereby genotoxicity in infants [81].
Gender-specific desensitization of group I metabotropic glutamate receptors after maternal L-glutamate intake during lactation
2018, International Journal of Developmental NeuroscienceDifferential effects of early-life NMDA receptor antagonism on aspartame-impaired insulin tolerance and behavior
2016, Physiology and BehaviorSecretions from placenta, after hypoxia/reoxygenation, can damage developing neurones of brain under experimental conditions
2014, Experimental NeurologyCitation Excerpt :Increasing the levels of systemic glutamate in the mother (outside the placenta) is known to cause a change in foetal brain receptors, neuronal survival and behaviour. According to some reports the glutamate passes across the placenta to reach the foetal brain (Takasaki, 1978; Yu etal., 1997, 2006; López-Zapata etal., 2011). Injections of glutamate analogues or NMDA antagonists or agonists into the maternal circulation will lead to neuronal degeneration and altered behaviour and parvalbumin staining in the brains of the offspring (Takai etal., 2003; Tanemura etal., 2009; Abekawa etal., 2011).