Although γ-aminobutyric acid (GABA) functions as an inhibitory neurotransmitter activating Cl− and K+ channels throughout the adult vertebrate central nervous system (CNS), recent evidence indicates that during embryonic and early post-natal development GABA excites CNS cells at spinal and supraspinal levels. Here we report that GABA promptly activates a transient Ca2+ conductance in cultured embryonic rat thalamic neurons that is mimicked by the GABAB receptor agonist (−) baclofen (BAC), but not the GABAA receptor agonist muscimol, and is blocked by the GABAB receptor antagonist saclofen, but not the GABAA receptor antagonists picrotoxin or bicuculline, which antagonize Cl− conductance. After 5-7 days in culture when functional networks have formed, GABA and BAC, but not muscimol trigger a flurry of synaptic-like transients, which reverse at the Cl− equilibrium potential, are blocked by bicuculline and decay with kinetics similar to those of GABAergic synaptic currents. This stimulatory effect desensitizes and is Ca2+-dependent. Taken together, the results indicate that exogenous GABA can trigger pulsatile transmission of endogenous GABA at GABAA receptors via activation of a presynaptic GABAB receptor-coupled, rapidly-decaying Ca2+ conductance. Since GABA emerges in cells and fibers during thalamic development, it may mediate developmentally important signals at both Cl− and Ca2+ channels.