GABA is the primary inhibitory neurotransmitter in adult mammalian brain. However, in neonatal animals activation of Cl^--permeable GABA receptors is excitatory and appears to depend on the expression of a Na⁺-K⁺-2Cl^- cotransporter (NKCC) that elevates intracellular Cl^- levels, leading to a depolarized Cl^- equilibrium potential (E_Cl). The change from excitation to inhibition appears to involve the expression of the K⁺/Cl^- co-transporter, KCC2, which lowers intracellular Cl^- levels resulting in a hyperpolarized E_Cl. In this study, we show that bovine chromaffin cells from four to five month old animals are excited by GABA. Activation of GABA_A receptors depolarizes the cells, opens voltage-dependent Ca²⁺ channels, elevates [Ca²⁺]_i and promotes the release of catecholamines. Blockade of voltage-dependent Ca²⁺ channels prevents the elevation of [Ca²⁺]_i by GABA. The extrapolated anion reversal potential in these cells is ~-28 mV indicating a resting intracellular anion concentration of ~50 mM. Expression of KCC2 protein was not detected in the juvenile chromaffin cells. In contrast, clear expression of NKCC1 was observed. Blockade of NKCC1 should reduce the intracellular Cl^- concentration and hyperpolarize E_Cl. Bumetanide, an NKCC1 blocker, reduced the elevation of [Ca²⁺]_i by GABA. In some cells activation of GABA_A receptors inhibits responses to excitatory neurotransmitters, even though GABA itself is depolarizing. Co-activation of cholinergic and GABA_A receptors in chromaffin cells produced elevations in [Ca²⁺]_i that were comparable to those produced by cholinergic receptors alone. Our data showing the selective expression of chloride co-transporters and the resulting strongly depolarized anion reversal potential may help explain how activation of GABA_A receptors causes sufficient excitation to elicit catecholamine release from chromaffin cells.