Lithium-potassium interaction in acutely treated cortical neurons and astrocytes.
Pure mouse primary cultures of cortical astrocytes and of cortical neurons were exposed to 1 mM Li+, i.e., a therapeutically relevant concentration. The 42K uptake rates of neurons were not influenced, whereas those of astrocytes showed an 11% inhibition (P less than 0.01). Internal loading with Li+ did not change the K+ uptake rates in either cell type. Neurons, which had been exposed for 5 min to veratridine, a situation which mimics neuronal activity, showed also no change in K+ uptake rate when Li+ was present during this time. Na+-K+ ATPase activity from cell homogenates was not changed in neuronal preparations by exposure to Li+, but astrocytic preparations appeared to show a slight increase by 14%. These experiments point out that the Li+ effects on ion distribution of the brain which have been described in the literature, are due to partly impairment of astrocytic K+ uptake. The mechanism of action, underlying the Li+ effect is probably a competition with K+ for transport sites at the external site of the Na+-K+ ATPase. This leads to a decrease of K+ uptake, but an enhancement of ATPase activity in the presence of Li+.
D000818:Animals; D001253:Astrocytes / Q000187:drug effects*; D002540:Cerebral Cortex / Q000187:drug effects*; D002712:Chlorides / Q000494:pharmacology*; D046508:Culture Techniques; D007473:Ion Channels / Q000187:drug effects; D008094:Lithium / Q000494:pharmacology*; D018021:Lithium Chloride; D051379:Mice; D009474:Neurons / Q000187:drug effects; D011188:Potassium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014701:Veratridine / Q000494:pharmacology
D002712:Chlorides; D007473:Ion Channels; D014701:Veratridine; D008094:Lithium; D000254:Sodium-Potassium-Exchanging ATPase; D018021:Lithium Chloride; D011188:Potassium