Selective vulnerability to kainate‐induced oxidative damage in different rat brain regions

Abstract

Some markers of oxidative injury were measured in different rat brain areas (hippocampus, cerebral cortex, striatum, hypothalamus, amygdala/piriform cortex and cerebellum) after the systemic administration of an excitotoxic dose of kainic acid (KA, 9 mg kg(-1) i.p.) at two different sampling times (24 and 48 h). Kainic acid was able to lower markedly (P < 0.05) the glutathione (GSH) levels in hippocampus, cerebellum and amygdala/piriform cortex (maximal reduction at 24 h). In a similar way, lipid peroxidation, as assessed by malonaldehyde and 4-hydroxyalkenal levels, significantly increased (P < 0.05) in hippocampus, cerebellum and amygdala/piriform cortex mainly at 24 h after KA. In addition, hippocampal superoxide dismutase (SOD) activity decreased significantly (P < 0.05) with respect to basal levels by 24 h after KA application. On the other hand, brain areas such as hypothalamus, striatum and cerebral cortex seem to be less susceptible to KA excitotoxicity. According to these findings, the pattern of oxidative injury induced by systemically administered KA seems to be highly region-specific. Further, our results have shown that a lower antioxidant status (GSH and SOD) seems not to play an important role in the selective vulnerability of certain brain regions because it correlates poorly with increases in markers of oxidative damage.

Oxidative stress in children affected by epileptic encephalopathies

“…Increased lipid peroxidation has been found in diverse brain areas of rats after picrotoxin-and pentylenetetrazole-induced seizures as well as in the kainic acidinduced seizure model [17][18][19][20]. In the electrically-induced convulsion model, the whole brain lipid peroxidation content was found to be increased in mice [21].…”

Alpha-lipoic acid affects the oxidative stress in various brain structures in mice with methionine and choline deficiency

“…CAT: catalase; GSH: glutathione; MCD: methionine-choline deficient; LA: lipoic acid; Cx: cortex; H: hypothalamus; S: striatum; Hipp: hippocampus ....................................................................................................................... previous studies. 44,45 Study by Candelario-Jalil et al showed that the hippocampus was the most vulnerable brain area to oxidative injury with respect to other areas in spite of showing a relatively high antioxidant capacity before kainate application. 44 In the same study, it was also shown that the levels of GSH and SOD may not correlate with an increase in lipid peroxidation.…”

Resveratrol Protects Against Neurotoxicity Induced by Kainic Acid

“…Since the CA1 and CA3 pyramidal neurons in the hippocampus and neurons in the hilar region of the DG are known to exhibit selective vulnerability to oxidative stress (10,11), special attention was focused on neurons in these brain areas (Fig. 1).…”

“…This neuroexcitant can bind to specific excitatory amino acid receptors in the brain (5). Activation of KA receptors is associated with an increase in the production of ROS and a sequalae of oxidative events (6)(7)(8)(9), including neuronal death in the hippocampal region (10,11). Therefore, neurodegeneration caused by systemic injection of KA has been widely used in studies to investigate possible pharmacological intervention against excitotoxic neurodegenerative disorders (4,12).…”