Adult primary afferent neurons are depolarized by GABA throughout their entire surface, including their somata located in dorsal root ganglia (DRG). Primary afferent depolarization (PAD) mediated by GABA released from spinal interneurons determines presynaptic inhibition, a key mechanism in somatosensory processing. The depolarization is due to Cl^- efflux through GABA_A channels; the outward Cl^- gradient is generated by a Na⁺,K⁺, 2Cl^- cotransporter (NKCC), as first established in amphibians. Using fluorescence imaging microscopy we measured [Cl^-]_i and cell water volume (CWV) in dissociated rat DRG neurons (P0-P21) loaded with MQAE and calcein respectively. Basal [Cl^-]_i was 44.2 ± 1.2 mM, Cl^- equilibrium potential (E_Cl was -27.0 ± 0.7 mV (n=75). This[Cl^-]_i is about four times higher than electrochemical equilibrium. Upon isosmotic removal of external Cl^-, cells loss Cl^- and shrank. Upon returning to control solution, cells reaccumulated Cl^- and recovered CWV. Cl^- reaccumulation had Na⁺-dependent (SD) and Na⁺-independent (SI) components. The SI component stabilized at [Cl^-]_i= 13.2 ± 1.2 mM, suggesting that it was passive (E_Cl = -60.5 ±3 mV). Bumetanide blocked CWV recovery and most (65%) of the SD-component (IC50 = 5.7 μM) indicating that both were mediated by NKCC. Active Cl^-uptake fell with increasing [Cl^-]_i and became negligible when [Cl^-]_ireached basal levels. The kinetics of active Cl^- uptake suggests a negative feedback system in which intracellular Cl^- regulates its own influx thereby keeping [Cl^-]_iconstant, above electrochemical equilibrium but below the value that would attain if NKCC reached thermodynamic equilibrium.