Na+,K(+)-ATPase activity is selectively increased in thalamus in thiamine deficiency prior to the appearance of neurological symptoms.
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.
Mousseau
D D
DD
Department of Psychiatry, Hôpital Saint-Luc (University of Montreal), Canada.
Rao
V L
VL
Butterworth
R F
RF
D000818:Animals; D002531:Cerebellum / Q000201:enzymology; D004791:Enzyme Inhibitors / Q000378:metabolism; D005493:Folic Acid Antagonists; D008297:Male; D010042:Ouabain / Q000378:metabolism; D011739:Pyrimethamine; D051381:Rats; D017207:Rats, Sprague-Dawley; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013788:Thalamus / Q000201:enzymology*; D013832:Thiamine Deficiency / Q000139:chemically induced / Q000201:enzymology*
D004791:Enzyme Inhibitors; D005493:Folic Acid Antagonists; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D011739:Pyrimethamine