GABA(b) receptors differentially regulate hippocampal CA1 excitatory synaptic transmission across postnatal development in the rat.

Depression of excitatory postsynaptic potentials (EPSPs) by the GABA(b) agonist, baclofen, was compared in hippocampal slices from juvenile (postnatal day (P) 15-21) and young adult (P28-35) rats. EPSP inhibition following baclofen application was not different between age groups, however, paired-pulse facilitation (PPF) increased more in young adults relative to juveniles. The differential effect of baclofen on PPF was not due to tonic receptor activity, since the GABA(b) antagonist, saclofen, did not differentially modify PPF. The baclofen-mediated increase in PPF for juvenile slices could be enhanced by first increasing transmitter release through an increased bath Ca2+ concentration. These findings suggests that ligand-mediated presynaptic depression is inversely related to the level of transmitter release and maturation of presynaptic inhibition is related to development of release.