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This research investigates how Na+,K+-ATPase inhibition by ouabain affects fear memory consolidation across specific brain regions.

May 9, 2026Open Access

Regional Crosstalk Between the Amygdala, Hippocampus, and Prefrontal Cortex Following Na+,K+-ATPase Inhibition by Ouabain

Key Points

This research investigates how Na+,K+-ATPase inhibition by ouabain affects fear memory consolidation across specific brain regions.
Ouabain infusion was administered, targeting Na+,K+-ATPase activity.
The activity and expression of α1 and β1 isoforms were measured after six hours.
Changes in oxidative stress markers and pro-inflammatory cytokine levels in the hippocampus and prefrontal cortex were analyzed.
Fear memory consolidation was specifically impaired in the basolateral amygdala (BLA).
Ouabain led to reduced catalytic activity and elevated pro-inflammatory cytokine expression.
Co-administration of D-serine did not alleviate the observed memory deficits.

Abstract

-ATPase inhibition in the BLA selectively impaired fear memory consolidation. Ouabain induced changes in Na⁺,K⁺-ATPase activity in the hippocampus and prefrontal cortex, and induces time-dependent upregulation of α1 and β1 isoforms. Six hours after infusion, ouabain triggered oxidative imbalance - characterized by reduced CAT activity. Pro-inflammatory cytokine expression was markedly elevated in the hippocampus and prefrontal cortex, while D-serine co-administration failed to rescue memory deficits. These findings establish a previously unrecognized role for Na⁺,K⁺-ATPase signaling in the BLA in coordinating the neurobiological processes essential for fear memory consolidation, indicating that its precise regulation is required for adaptive fear memory formation.

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