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We have studied the effect of serotonin on synaptic transmission in rat hippocampal subiculum slices. Electrical stimulation of the alveus induced a field potential in the subiculum. The non-NMDA glutamate receptor antagonist, NBQX (3 x 10(-6) mol/l) suppressed the response by 78%, indicating that the signal involves glutamatergic neurons. Application of serotonin suppressed (EC50 = 3.6 x 10(-6) mol/l) the amplitude of the evoked potentials in a reversible, concentration-dependent manner. The responses to 5-HT were not altered after pretreatment with the 5-HT uptake blocker, fluvoxamine (10(-5) mol/l) or a combination of the MAO inhibitor pargyline (10(-5) mol/l) and ascorbic acid (10(-4) mol/l). The responses to 5-HT were also unaffected by pretreatment with the 5-HT1A selective antagonist NAN-190 (10(-6) mol/l), the 5-HT2A antagonist ketanserin (10(-6) mol/l) or the 5-HT3/5-HT4 antagonist ICS 205-930 (10(-6) mol/l). The 5-HT1B selective agonist CP 93,129 mimicked the effects of serotonin, but was more potent (EC50 4.1 x 10(-7) mol/l). The 5-HT1B receptor antagonist, (+/-)21-009 (3 x 10(-7) mol/l), antagonized the response to 5-HT and CP 93,129 with a pKB value of 7.1 and 7.2, respectively. These results suggest that the effect of 5-HT in the rat subiculum is mediated by 5-HT1B receptors.

Among the various molecular events that have been proposed to contribute to the mechanisms of long-term potentiation (LTP), one of the most cited possibilities has been the activation of protein kinase C (PKC). Here we review various aspects of the cellular actions of PKC activation and inhibition, with special emphasis on the effects of the kinase on synaptic transmission and the N-methyl-D-aspartate (NMDA) and non-NMDA receptor-mediated components of synaptic responses. We discuss the implications of these effects for interpretations of the role of PKC in the mechanisms of LTP induction and maintenance.

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