Abstract
The present study was carried out to investigate the effect of NMDA, bicuculline and kainic acid (KA) on the extracellular concentration of glutathione, phosphoethanolamine (PEA) and taurine in rat hippocampus in vivo. Rats were implanted with intrahippocampal microelectrodes perfused with free-glucose Krebs-Ringer solution and allowed to recover for about 2 h. After assaying baseline concentrations of amino acids, NMDA or bicuculline was administered intrahippocampally, whereas KA was given systemically. Either treatment resulted in significant high extracellular concentrations of glutathione, but only NMDA or KA resulted in high concentrations of PEA and taurine. Interestingly, the increase in glutathione concentration due to KA was followed by a delayed increase of glutamate and PEA. Our results demonstrated that increased efflux of glutathione, a common consequence of different neuroexcitotoxic agents, occurs in vivo. Given that the agents used in the present study were also convulsunts, the implication of the findings on seizure predisposition was also considered.
Highlights
Glutathione, a tripeptide of glutamate, cysteine and glycine, displays high intracellular concentrations [1] [2]
A significant high concentration of the tripeptide continued throughout the first 100 min following single kainic acid (KA) injection (Figure 1(a)) while the increase remains high throughout the whole experiment after continuous NMDA perfusion (Figure 1(b))
Results without acivicin addition (Figures 1(a)-(c)) reveal less concentration of glutathione than with acivicin addition (Figure 2(a)), there was still no difference in the pattern of glutathione elevation between the groups, with exception of that under KA treatment the glutathione concentration was significantly high during the last fraction, i.e. at 120 min (Figure 2(a) vs. Figure 1(a))
Summary
Glutathione, a tripeptide of glutamate, cysteine and glycine, displays high intracellular concentrations [1] [2]. This high concentration can be related to its functions in maintaining the overall reduction-oxidation potential states of neural cells [2] and protecting them against oxidative damage [3] [4]. Abbas functions in all cell types, much evidence shows that its extracellular [5] and/or intracellular [6] pool might act, in the brain, as a neurotransmitter/neuromodulator via different mechanisms [7] like enhancement of NMDA receptors function and contribution in synaptic plasticity such as LTP [8] [9]. A generalized underlying mechanism for these acute and chronic neurological diseases may be partly mediated by oxidative stress caused by overactivation of glutamate receptors [12]
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