Activation of presynaptic ␥-aminobutyric acid type B (GABA B ) receptors inhibits neurotransmitter release at many synapses (both excitatory and inhibitory), and activation of postsynaptic GABA B receptors leads to a general inhibition of the postsynaptic cell in mature neurons. Although the action of GABA B receptors at the soma of excitatory hippocampal pyramidal cells has been resolved to be regulation of a potassium or calcium conductance, it is not clear that all neurons in the hippocampus demonstrate similar effects of GABA B receptor activation. In the current study, GABA B receptormediated effects on calcium currents in acute cultures composed of heterogeneous cells from the superior region of neonatal hippocampi were studied. In 54.5% of cells, the GABA B receptor agonist baclofen (10 M) attenuated the whole-cell calcium current by 21.0% Ϯ 1.1%. In 29.9% of cells, baclofen facilitated the calcium current by 43.5% Ϯ 8.1%. The component of current attenuated by baclofen was blocked by the N-type calcium channel antagonist -conotoxin GVIA (3 M). The component of current facilitated by baclofen was blocked by the L-type channel antagonist nimodipine (20 M). For cells that showed calcium current facilitation, baclofen shifted the half-maximal activation by approximately -14 mV. The data indicate that activation of GABA B receptors in neurons of the superior hippocampus attenuates current through N-type channels and facilitates current through L-type channels. The two opposing effects of GABA B receptor activation may reflect the heterogeneity of the cultured cells or may be a developmentally regulated phenomenon.