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

Abstract

Changes in the activity of Na+,K+-ATPase and in the water, Na+, and K+ levels in the parietal cortex, hippocampus, and thalamus were investigated in rats 1, 3, 6, and 24 h following systemic kainic acid injection. An increase in Na+,K+-ATPase activity was observed in all three regions 3 h after the treatment, with a subsequent decrease in enzyme activity. The elevation in Na+,K+-ATPase activity was accompanied by an increase in the Na+ content and a decrease in the K+ content. These changes are presumed to occur because of repeated discharges and excessive prolonged depolarization in response to kainic acid. The decreases in Na+,K+-ATPase activity 6 and 24 h following kainic acid treatment coincide with neuropathological damage and edema formation, mainly in the hippocampus and thalamus.

The importance of systemic response in the pathobiology of blast-induced neurotrauma

“…Changes in Na + , K + -ATPase have been shown being time-dependent (Sztriha et al, 1987), and in the present study the activity Na + , K + -ATPase was measured at the time when significant neuro-endocrine changes occur in the brain with TBI. Indeed, complex alterations such as the over-activation or inhibition of neurotransmitter synthesis, release, or transport have been reported during the early period after TBI (McIntosh et al, 1994).…”

“…The Na + , K + -ATPase activity change is an excellent example demonstrating the duality of response mechanisms to injury where increased and reversible activity after various brain insults in animals during the acute (<3 h) post-injury period (MacMillan, 1982; Goldberg et al, 1984; Sztriha et al, 1987) is followed by reduced activity during the chronic post-injury period (Jovicic et al, 2008; Crema et al, 2010) potentially leading to irreversible neurodegenerative central nervous system disorders (Seddik et al, 1991; Kumar and Kurup, 2002; Lima et al, 2008). While the Na + , K + -ATPase activity is not disease specific, its phase-dependent activity change as well as its kinetic profile to ATP might be a useful indicator of the BINT development and progress.…”

Quinazoline-based tricyclic compounds that regulate programmed cell death, induce neuronal differentiation, and are curative in animal models for excitotoxicity and hereditary brain disease

“…These models included systemic kainic acid injections in rats to induce localized excitotoxic damage in hippocampus, amygdala, and pyriform cortex, and subsequent edemic damage spread throughout the brain. 43 , 45–48 We also studied the R6-2 transgenic mouse model for the human hereditary neurodegenerative disease of Huntington, which presents damage in the striatum and cortex, motor disturbances, and finally, early death. 49 , 50 Thus, we endeavored to find out whether these tricyclic compounds based on a quinazoline scaffold could counteract the damage and behavioral deficits and potentially even restore the aberrant behavior to normal.…”

Changes in Cholinergic but Not in GABAergic Markers in Amygdala, Piriform Cortex, and Nucleus Basalis of the Rat Brain Following Systemic Administration of Kainic Acid

“…Changes in the water, sodium, and potassium contents as well as in the Na+, K+-ATPase activity of various brain regions have been reported after systemic injection of kainic acid in the rat (Korf and Postema, 1984;Sztriha et al, 1986Sztriha et al, , 1987. Recent investigations in this animal model have also revealed marked changes in brain tissue of the level and turnover of noradrenaline, dopamine, and serotonin (Sperk et al,198 l), in levels of extracellular amino acids (Wade et al, 1987), in the activities of glutamic acid decarboxylase and choline acetyltransferase (ChAT) (Sperk et al, , 1985, in the uptake of glutamate (Heggli et al, 1981;Heggli and Malthe-Ssrenssen, 1982), and in benzodiazepine and y-aminobutyric acid (GABA) receptor binding , which were restricted only to some structures, such as the hippocampus, amygdala, and piriform cortex.…”