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Electrophysiological and pharmacological data suggested that 5-HT(1B) receptors mediate enhancement of excitatory postsynaptic responses induced by NMDA in hippocampal slices. The aim of this study was to clarify whether modulation of the NMDA receptor by 5-HT(1B) receptors involves different pathways in the postsynaptic interneurons. In CA1 neurons, 5-HT(1B) receptor activation enhanced NMDA-induced responses. This enhancement was mimicked by direct activation of 5-HT(1B) receptors with the full agonist CP94253, but not with the partial agonist GR125743. Such a non-selective 5-HT(1B/1D) receptor agonist induced no response in its own, but amplified the NMDA-induced response in a concentration-dependent manner. Pertussis toxin abolished the CP94253-induced amplification. NMDA activation caused a small cGMP elevation, whereas CP94253 in the same concentration range caused a concentration-dependent cGMP increase. GR125743-induced cGMP rise was smaller than that induced by NMDA stimulation. A combination of the two agents resulted in an additive effect on cGMP rise. These data indicate that NMDA-induced cAMP rise is largely due to activation of postsynaptic adenylyl cyclase. On the other hand, the CP94253-induced cAMP rise was mainly due to activation of a Gi/Go-protein coupled receptor. Modulation of NMDA responses in CA1 neurons by 5-HT(1B) receptors appears to involve participation of both adenylyl cyclase and guanylyl