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  • Na K ATPase adenosine triphosphate ATP and astrocytic glutam


    Na+/K+-ATPase, (+)- Corydaline and astrocytic glutamate transporters act together to maintain sodium and potassium gradients and the proper activities of EAAT1 and EAAT2 (Rose et al., 2009; Sheean et al., 2013); nevertheless, in present study, Na+/K+-ATPase activity was shown to be increased as from 24 h. It is possible to suggest that such augmented activity is a compensatory mechanism to reduce the extracellular potassium content and to decrease the electrical stimulation caused by the changes in electrolytes distribution (Kinjo et al., 2007; Yang et al., 1994). Moreover, glycolytic enzymes and mitochondria are also required to support astrocytic glutamate uptake (Genda et al., 2011; Sheean et al., 2013). Genda et al. (2011) demonstrated that either glycolysis or oxidative phosphorylation are sufficient to support transport, but when both are inhibited, glutamate transport is severely compromised (Genda et al., 2011). Thus, it is possible that the acute energetic demand imposed after the event caused the partial inhibition of EAAT1 and EAAT2, whereas the augmented Na+/K+-ATPase activity could be partially responsible for the increased EAAT2 expression. An increase of EAAT2 is reported to exert significant neuroprotective effects 7 days after focal cerebral ischemia (Fontana, 2015; Harvey et al., 2011). Yatomi et al. (2013) showed that chronic cerebral hypoperfusion resulted in a transient up-regulation of glial glutamate transporter EAAT2 (Yatomi et al., 2013). Likewise, several reports show distinct changes in the EAAT's expression patterns according to the protocol of brain lesion (Martinez-Lozada et al., 2016; Sánchez-Mendoza et al., 2010). The ROCK/Rho system seems to play a major role in determining the cell surface expression of EAAT1/2 and interfere with astrocytic morphology, contractility, migration, proliferation and survival (Lau et al., 2011; Pellegrin and Mellor, 2007; Riento and Ridley, 2003). Therefore, considering the diversity of aforementioned results, the differential contribution of EAAT1 and EAAT2 expression to brain ischemia remains to be elucidated.
    Introduction Nowadays it is estimated that human daily consumed between 30–200 mg /Kg of l-Glutamate (l-Glu) (Beyreuther et al., 2007; Fernandez-Tresguerres Hernández, 2005; He et al., 2011). An important contributor to l-Glu intake is monosodium glutamate a food additive widely used to increase the flavor of the food (Halpern, 2000). Since several researchers in the 70´s showed neuronal necrosis following l-Glu administration (Burde et al., 1971; Olney and Sharpe, 1969), the neurotoxicity of this aminoacid has been intensively studied, especially in the first stages of life. Thus, a consensus meeting on safety of monosodium glutamate on 2007 stated that placental barrier avoid the passage of glutamate from maternal plasma to fetusses (Beyreuther et al., 2007). There are, however, evidence that suggest that glutamate passes to circulation and finally may reach Central Nervous System (CNS) of fetusses following maternal oral consumption of l-Glu (Hermanussen et al., 2006). Concerning lactation period, the effect of maternal oral consumption of l-Glu on suckling babies remains elusive. It is known, however, that maternal milk contains large amounts of free aminoacids (Baldeón et al., 2014), especially glutamate and glutamine which represent nearly of 50% of total (Agostoni et al., 2000; Chuang et al., 2005; Elmastas et al., 2008; Sarwar, 2001) and some investigators have also suggested that maternal diet may change the concentration of free aminoacids in breast milk (Lindblad and Rahimtoola, 1974; Wurtman and Fernstrom, 1979). Although the role of free aminoacids in maternal milk is not completely understood, it is suggested that glutamate may play a relevant role in the growth and development of breast-fed infant by acting as neurotransmitter in the brain among others functions (Zhang et al., 2013). In the CNS l-Glu acts as an excitatory neurotransmitter being involved in key brain processes such as development, learning and memory formation. The actions of l-Glu are mediated by a group of membrane receptors named glutamate receptors which include ionotropic (iGluRs) and metabotropic (mGluRs) glutamate receptors. iGluRs are ligand-gated ion channels responsible for fast excitatory neurotransmission and which have been further subdivided into three types (AMPA, NMDA and Kainate) according to the response to agonist. mGluRs belong to G-protein coupled receptor (GPCR) superfamily and have been subclassified into three groups: Group I (mGluR1 and mGluR5) which stimulate phospholipase C (PLC) activity through a Gq/11 protein, Group II (mGluR2 and mGluR3) and Group III (mGluR4, mGluR6, mGluR7 and mGluR8) which inhibit adenylyl cyclase (AC) activity through a Gi/o protein (Pin and Acher, 2002; Pin et al., 2003). mGluRs are distributed throughout CNS where modulate neuronal excitability and synaptic transmission (Niswender and Conn, 2010). The activity of group I-mGluR is significantly increased in developing brain which allowed to suggest that group I-mGluR could play a relevant role during brain development (Romano et al., 1996).