Late maturation of GABA B synaptic transmission in area CA1 of the rat hippocampus

Abstract

Whole cell voltage clamp recordings were used to investigate the postnatal development of GABA B synaptic transmission in CA1 pyramidal cells of rat hippocampal slices. In the presence of antagonists of glutamate and GABA A ionotropic receptors, electrical stimulation evoked slow IPSCs in pyramidal cells from mature animals (35–45 days postnatal, P35–45). Brief trains of stimulation evoked slow IPSCs of greater magnitude. I–V relations of slow IPSCs were inwardly rectifying, with a mean equilibrium potential near −75 to −80 mV. Slow IPSCs were completely antagonized by the GABA B antagonist CGP55845A (0.5 μM). In cells from young animals (P12–14), similar stimulation evoked either no or very small slow IPSCs (mean conductance ∼10% of adult). In cells from animals of intermediate age (P22–24), slow IPSCs were more frequent and their mean conductance was ∼60–80% of adult values. Bath application of 20 μM baclofen evoked outward currents in cells of animals P35–45. I–V relations of baclofen currents showed inward rectification and reversed near −80 mV. Baclofen currents were absent or minimal in animals P12–14, and of intermediate magnitude in animals P22–24. These results indicate that baclofen and GABA B postsynaptic currents are virtually absent 2 weeks postnatally, and appear gradually until 35–45 days postnatal. Thus, GABA B synaptic transmission appears to mature late in area CA1 of the rat hippocampus.