Stabilization of serotonergic neurotransmission by depressing the activity of serotonergic neurons may be the common mode of action of drugs effective in migraine. By serotonin receptor agonism, by prolonging the biologic half-life of serotonin in the synaptic cleft (through blockade of its re-uptake or metabolic degradation), by an increase in its synthesis, by inhibiting the release of serotonin, or by activation of cyclic AMP (fig), a unitary expression for the action of these drugs can be formulated which is corroborated, for many of the drugs, by direct measurement of serotonergic neuronal firing rates. However, there are at least three serotonin receptor sites in brain at which drugs would be effective, as assessed by differential responsiveness to agonists and antagonists and by different types of postsynaptic responses: presynaptically, postsynaptically, and at the autoreceptor itself. The locus of action for the antimigraine drugs may be primarily at the raphe, upon the serotonin neurons per se, but it will probably prove to be more complex as more data are generated.
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