PMC

1. Potassium chloride in calcium chloride solution.
2. Sodium chloride in calcium chloride solution.
3. Potassium chloride in barium chloride solution.
4. Sodium chloride in barium chloride solution.
5. Barium chloride in sodium chloride solution.
6. Calcium chloride in sodium chloride solution.
7. Barium chloride in potassium chloride solution.
8. Calcium chloride in potassium chloride solution.

○, recovery from chloride depletion; •, recovery from chloride loading. A, time course of recovery of GABA reversal potential. B, time course of recovery of chloride equilibrium potential. C, time course of recovery of intracellular chloride concentration. The resting chloride concentration (▴) was about 9.5 mm. D, time course of recovery of absolute change in [Cl⁻] _i. The resting chloride concentration was subtracted from the data shown in C. Two exponential curves with time constants of 8.83 s (chloride loading) and 2.4 s (chloride depletion) were fitted to the results.

DSF/Cu activated chloride currents in LNCaP cells suppressed by NPPB and DIDS. A, Full‐process diagram of DSF/Cu‐activated LNCaP chloride currents suppressed by DIDS. B, Instantaneous diagram of DSF/Cu‐activated LNCaP chloride currents. C, Instantaneous diagram of DSF/Cu‐activated LNCaP chloride currents suppressed by DIDS. D, I‐V curve of DSF/Cu‐activated LNCaP chloride currents suppressed by DIDS. E, Statistics diagram of I‐V relationship between DSF/Cu‐activated chloride currents and DIDS‐suppressed currents (**P < .01, n = 3). F, Full‐process diagram of DSF/Cu‐induced LNCaP chloride currents suppressed by NPPB. G, Instantaneous diagram of DSF/Cu‐activated LNCaP chloride currents. H, Instantaneous diagram of DSF/Cu‐activated LNCaP chloride currents suppressed by NPPB. I, I‐V curve of DSF/Cu‐activated LNCaP chloride currents suppressed by NPPB. J, Statistical diagram of I‐V relationship between DSF/Cu‐activated chloride currents and NPPB‐suppressed currents (**P < .01, n = 3) [Colour figure can be viewed at wileyonlinelibrary.com]

Neonatal inflammation impairs chloride extrusion in adult, male CA1 pyramidal neurons. A, Chloride transporters NKCC1 and KCC2 regulate chloride levels in neurons. NKCC1 is primarily expressed during young ages and shuttles chloride into cells. KCC2 is primarily expressed in adulthood and extrudes chloride. The direction of chloride flow through the GABA-A receptor, a ligand-gated chloride channel, is determined by transporter-defined, intracellular chloride levels. B, Neonatal inflammation leads to elevated chloride levels in adult CA1 pyramidal neurons, but only in males. Abnormal NKCC1 activity is proposed to promote high chloride levels in adult, male CA1 pyramidal neurons. Shapes representing NKCC1 KCC2 and chloride are similar to those depicted in panel A.