, 2007, Binder and Steinhauser, 2006, Zhang et al , 2004, Ueda et

, 2007, Binder and Steinhauser, 2006, Zhang et al., 2004, Ueda et al., 2001 and Tanaka et al., 1997). Glutamate, after being taken up into astrocytes, may be converted to glutamine

by glutamine synthetase (GS), which then is released to extracellular space and taken up by neurons where it is converted again to glutamate and stored in pre synaptic vesicles (Danbolt, 2001 and Suarez et al., 2002). Thus, the GS activity is an essential step in the glutamate–glutamine cycle, and its impairment has been implicated in pathogenesis of temporal lobe epilepsy (TLE), since GS expression and activity is reduced in the hippocampus of TLE patients (Eid et al., 2004). In adult animals, GS was increased in the latent phase and decreased in the chronic phase of kainate-induced seizures (Hammer et al., 2008). The consequences VEGFR inhibitor of status epilepticus (SE) in the developing brain appear to be different from those of mature brain. Comparisons of the findings obtained in the adult and newborn brain reveal a paradox, in that the immature brain has generally been considered ‘Libraries resistant’ to the damaging

Angiogenesis inhibitor effects of hypoxia and hypoxia–ischemia, while at the same time exhibiting periods of heightened sensitivity to injury, dependent on the specific developmental stage of the brain ( Holmes, 2005 and Hurn et al., 2005). Despite science that, the immature brain is not immune to

injury in prolonged seizure as SE. Changes in AMPA receptors and EAAC1 transporter expression were reported in SE rats at 10 days post-natal (P10) and these modifications were related to higher susceptibility to another seizure episode (Zhang et al., 2004). Despite the apparent low susceptibility of immature brain to seizure-induced cell death, seizures in the developing brain can result in irreversible alterations in neuronal connectivity (Holmes and Ben-Ari, 2001). Neonatal rats, which suffered from SE displayed synaptic alterations and memory impairment in the adulthood (Cognato et al., 2010, Cornejo et al., 2007 and Cornejo et al., 2008), showing that disturbances in a critical period of brain maturation could persistently compromise its function. Furthermore, neural injuries such as hypoxic or hypoxic–ischemic insult to the developing brain will impact on subsequent maturation, with long-lasting consequences for the adult brain (Hurn et al., 2005). Although some information is available regarding the involvement of glutamate transporters in events triggered by seizure activity in adult animals (Rothstein et al., 1996, Ueda et al., 2001, Simantov et al., 1999 and Miller et al., 1997), little is known about the neonatal brain responses to seizure involving glutamate transporters, especially in the early period post-seizure.

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