THE hippocampus contains interneurons that release gamma-aminobutyric
acid (GABA). GABA hyperpolarizes hippocampal CA1 and CA3 pyramidal cel
ls through activation of GABA(B) postsynaptic receptors. GABA(B) and 5
-hydroxytryptamine(1A) (5-HT1A) receptors share effector mechanism(s).
Agonist potency and the maximal hyperpolarization produced by 5-HT1A
receptor activation is different between the CAI and CA3 subfields. We
determined that baclofen, a selective GABA(B) agonist, was more poten
t and produced a greater maximal response in area CA3 than in CAI. The
larger magnitude of the response can be attributed partly to the larg
er input resistance of CA3 neurons. GABA(B) receptor-effector coupling
differences between area CAI and CA3 are proposed as the mechanism un
derlying the baclofen response incongruities.