Na +,K +-ATPase activity is selectively increased in thalamus in thiamine deficiency prior to the appearance of neurological symptoms

Abstract

The relationship between progression of neurological status and the activities of both Na +,K +- and Mg 2+-dependent-ATPase (adenosine 5′-triphosphate phosphohydrolase) was investigated in brain regions of pyrithiamine-induced thiamine deficient rats. Thalamic Na +,K +-ATPase activity was selectively increased by 200% ( P < 0.01) prior to the appearance of symptoms of thiamine deficiency and normalized in symptomatic rats. This selective transitory activation precludes a mediation by brain soluble fraction Na +,K +-ATPase modifiers as does the unaltered distribution in regional high-affinity [ 3H]ouabain binding densities observed throughout the time-course used in these experiments. Na +,K +-ATPase maintains cellular ionic gradients and has been implicated in neurotransmitter uptake and release mechanisms. The fact that the increased thalamic Na +,K +-ATPase activity coincides with the early alterations in serotonin metabolism observed in similarly treated animals and the concomitantly early increase in glucose utilization previously observed in the thalamus of thiamine-deficient rats is discussed.