Active transport of chloride by the giant neuron of the Aplysia abdominal ganglion.
Internal chloride activity, a(i) (Cl), and membrane potential, E(m), were measured simultaneously in 120 R2 giant neurons of Aplysia californica. a(i) (Cl) was 37.0 +/- 0.8 mM, E(m) was -49.3 +/- 0.4 mv, and E(Cl) calculated using the Nernst equation was -56.2 +/- 0.5 mv. Such values were maintained for as long as 6 hr of continuous recording in untreated neurons. Cooling to 1 degrees -4 degrees C caused a(i) (Cl) to increase at such a rate that 30-80 min after cooling began, E(Cl) equalled E(m). The two then remained equal for as long as 6 hr. Rewarming to 20 degrees C caused a(i) (Cl) to decline, and E(Cl) became more negative than E(m) once again. Exposure to 100 mM K(+)-artificial seawater caused a rapid increase of a(i) (Cl). Upon return to control seawater, a(i) (Cl) declined despite an unfavorable electrochemical gradient and returned to its control values. Therefore, we conclude that chloride is actively transported out of this neuron. The effects of ouabain and 2,4-dinitrophenol were consistent with a partial inhibitory effect. Chloride permeability calculated from net chloride flux using the constant field equation ranged from 4.0 to 36 x 10(-8) cm/sec.
D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism*; D003080:Cold Temperature; D004140:Dinitrophenols / Q000494:pharmacology; D008564:Membrane Potentials; D008839:Microelectrodes; D008974:Mollusca / Q000502:physiology*; D009433:Neural Inhibition / Q000187:drug effects; D009474:Neurons / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D012623:Seawater
D002712:Chlorides; D004140:Dinitrophenols; D010042:Ouabain; D000109:Acetylcholine; D011188:Potassium