In Figure 10 of D'Amico et al. (2014) the KCC2 co-transporter was incorrectly drawn as a co-exchanger. This has been corrected in this version of the figure to show that both chloride and potassium are pumped out of the motoneuron.
Figure 10.
KCC2 cotransporter and chloride equilibrium before and after SCI. (A) A potassium chloride cotransporter (KCC2) transports both chloride (Cl−) and potassium (K+) out of the motoneuron (MN) to maintain Cl− equilibrium potential below resting membrane potential, allowing Cl− influx and MN hyperpolarization during activation of GABA and Glycine receptors (R). (B) Downregulation of KCC2 expression in motoneurons after SCI increases intracellular Cl− concentration, depolarizing Cl− equilibrium potential to above rest. This produces efflux of Cl− and depolarization of MN during activation of GABA and Glycine receptors. Activation of 5-HT2A receptors increases cell membrane expression of KCC2 after SCI to restore endogenous inhibition.
Conflict of interest statement
The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.