Abstract
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 Ca 2+ 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.
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