Inhibition by sumatriptan of central trigeminal neurones only after blood‐brain barrier disruption

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Abstract
1 The 5-hydroxytryptamine (5-HT1)-like agonist, sumatriptan, is highly efficient in the relief of migraine headache and its accompanying symptoms. 2 Experimental evidence has indicated that its site of action may be on the cranial vessels or on the trigeminal innervation of the cranium, or both, since sumatriptan does not pass the blood-brain barrier easily under normal circumstances. It is, however, not clear whether the blood-brain barrier is normal or abnormal during a migraine attack. 3 In this study, single unit activity and trigeminal somatosensory evoked potentials in central trigeminal neurones were monitored during electrical stimulation of the superior sagittal sinus. 4 Intravenous administration of sumatriptan (100 μg kg−1) did not alter trigeminal evoked activity unless the permeability of the blood-brain barrier had been increased by infusion of an hyperosmolar mannitol solution. After blood-brain barrier disruption, sumatriptan decreased the peak-to-peak amplitude of evoked potentials by 40 ± 6% and the probability of firing of single units by 30 ± 9%. Mannitol infusions alone in control animals caused no changes in evoked potentials or single unit activity. 5 The data suggest that in normal circumstances sumatriptan does not have sufficient access to trigeminal neurones to alter their function.