Abstract
Objective: Our previous studies have revealed that ferulic acid (FA) and sodium ferulate (SF) show significant protective effect on excitotoxicity, the present study was conducted to compare its potential favorable effects of maternal，newborn，and both maternal and newborn intraperitoneal (ip) injection of SF on repair following excitotoxic neuronal damages induced by monosodium glutamate (MSG). Methods: The maternal mice were assigned randomly into seven groups (n = 10 animals in each group): control, 3SF, 20SF, 23SF, MSG, MSG + 3SF, MSG + 20SF, MSG + 23SF groups. The mice at 17 days of pregnancy were treated with or without MSG (2.0 g/kg body weight, ig, once) or/and SF (40 mg/kg body weight, ip), and their offerings treated with or without SF. And then their filial behaviors and hippocampal histopathology were studied. Results: The results showed that maternal, newborn, and both maternal and newborn administration of SF facilitated their filial brain repair, and attenuated the behavioral disorders and histopathological damages of their filial mice in MSG + 3SF, MSG + 20SF, and MSG + 23SF groups in varying degrees. However, the best effects were detected in the filial mice in MSG + 23SF group. Conclusion: Both maternal and newborn administration of SF is conducive to the filial neuronal repair following excitotoxic damages induced by glutamate.
Highlights
Excitatory amino acids (EAAs) are utilized by nearly every information—bearing circuit in the brain, and during development
These findings suggest that sodium ferulate (SF) had no obvious effect on locomotion and exploration, rather than, countered the effect of monosodium glutamate (MSG) on those of the filial mice from mothers treated with MSG
The development of mice is an example of experimental mammalian embryology, and mouse development is the basis for the study of human ontogeny
Summary
Excitatory amino acids (EAAs) are utilized by nearly every information—bearing circuit in the brain, and during development. EAAs play a pivotal role in learning, memory, and brain plasticity. Exitotoxicity, defined as excessive exposure to the neurotransmitter glutamate or overstimulation of its membrane receptors, has been implicated as one of the key factors constributing to neuronal injury and death in a wide range of both acute and chronic neurodegenerative disorders. Neurodegenerative disorders, including Alzheimer’s disease, Parkingson’s disease, Huntington’s chorea, HIV-associated dementia, multiple sclerosis, amyotrophic lateral sclerosis, and glaucoma, are caused by different mechanisms but may share a final common pathway to neuronal injury due to overstimulation of glutamate receptors, especially of the N-methyl-D-aspartate (NMDA) subtype [5]. We have successfully established an experimental model of excito-toxic brain injury following exposure to glutamate, in which maternal ig excessive administration of MSG at a late stage of pregnancy results in a series of behavioral disorders, and obvious histopathological brain lesion in their offspring [6,7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
