The electrogenic effects of Na(+)-K(+)-ATPase in rat auditory thalamus.
1. The electrogenic effects of the Na(+)-K(+)-ATPase in thalamic neurones were investigated by means of intracellular and whole-cell patch-clamp recording techniques in rat medial geniculate body (MGB) maintained in vitro. 2. In twenty-six out of thirty-one neurones recorded intracellularly, application of the Na(+)-K+ pump inhibitor strophanthidin induced two different types of membrane depolarization: a small, reversible depolarization with a peak amplitude of 4 +/- 2.6 mV or a prolonged depolarization of large amplitude (48.6 +/- 9.0 mV) with or without a decrease in apparent membrane resistance. Blockade of glutamate receptors with kynurenic acid or 6-cyano-7-nitroquinoxaline-2,3-dione and (+/-)-2-amino-5-phosphonopentanoic acid did not prevent either type of pump response, but the large depolarization was not seen when the medium contained the sodium channel blocker TTX. 3. Whole-cell patch-clamp recording showed that the small membrane depolarization is mediated by an inward membrane current (39.00 +/- 5.70 pA) that exhibited a weak voltage dependence. An inward current of similar amplitude was also induced in MGB cells when the pipette solution contained nominally zero Na+ or when K+ was temporarily omitted from the extracellular medium. The large membrane depolarization or the corresponding membrane current was not observed in whole-cell conditions. 6. Transient inhibition of the electrogenic Na(+)-K(+)-ATPase consistently led to a change in the mode of synaptic transmission in MGB cells, during which the synaptically evoked burst response was either blocked or converted into a single spike discharge. 7. Taken together, these data suggest that blockade of the electrogenic pump produces a dual membrane effect in mammalian thalamic neurones: a small electrogenic membrane depolarization and a large depolarization response that can be prevented by artificially maintaining the transmembrane ionic gradients. The electrogenic activity of the Na(+)-K(+)-ATPase may play an important role in setting the mode of synaptic transmission in sensory thalamus.
Senatorov
V V
VV
Loeb Medical Research Institute, Ottawa Civic Hospital, University of Ottawa, Ontario, Canada.
Mooney
D
D
Hu
B
B
D000818:Animals; D001306:Auditory Pathways; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D005071:Evoked Potentials / Q000187:drug effects; D005829:Geniculate Bodies / Q000201:enzymology / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008954:Models, Biological; D009474:Neurons / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D009924:Organ Culture Techniques; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013327:Strophanthidin / Q000494:pharmacology*
D013327:Strophanthidin; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium