Kainic acid neurotoxicity: Characterization of blood-brain barrier damage

Brain reactive antibodies and the blood-brain barrier: Observations in aging rodents and the effects of peripheral kainic acid

“…The involvement of glutamate or aspartate neurons in hippocampal damage following KA has been suggested [37]. The role of such cells in AD has not been fully evaluated.…”

“…The damage following peripheral administration of KA has been reported to be especially notable in the piriform cortex and the hippocampal pyramidal cell layer (161 and in layer I11 of entorhinal cortex [33]. Blood-brain barrier disruption following peripheral KA is most notable in the thalamus [37], in olfactory cortex, amygdala, hippocampus, thalamus, and neocortex [33], or in septum, hippocampus, hypothalamus, piriform cortex, amygdala, and entorhinal cortex [42]. The mechanism by which KA damages the barrier appears to be related both to an increase in peripheral blood pressure and to an induction of seizure activity [29; 37; 421.…”

“…Seizures without a blood pressure increase [29] or a blood pressure increase alone [29; 371 were not sufficient to open the blood-brain barrier. The barrier damage in the thalamus and septum may be due to firing of affected hippocampal neurons which project to these brain regions [37].…”

Effects of Systemic Kainic Acid Administration on Regional Na+, K+‐ATPase Activity in Rat Brain

“…The decrease in Na+,K+-ATPase activity during the late period (after 3 h) following KA administration coincides with the necrobiotic processes (Schwob et al, 1980) and edema formation caused by KA (Sztriha et al, 1985(Sztriha et al, , 1986a. Neuropathological damage has been consistently observed in the hippocampal formation, thalamic nuclei, and certain parts of the neocortex 2 4 h after KA injection (Schwob et al, 1980).…”

“…Kainic acid (KA) administered systemically causes convulsions resembling human temporal lobe epilepsy; the seizure activity has been proven to last for days (Ben-Ari, 1985), and typical neuropathological alterations have been observed after KA administration (Schwob et al, 1980). Changes in the water, sodium, and potassium contents of various brain regions have been reported after local or systemic injection of KA (Korf and Postema, 1984;Sztriha et al, 1985Sztriha et al, , 1986b. It is accepted that membrane-bound Na',K'-ATPase plays an important role in the active transport of Na' and K' , maintaining cellular ionic gradients and membrane potentials.…”