Panteleev S S, Sokolov A Yu, Kartus D E, Amelin A V, Ignatov Yu D
I. P. Pavlov Institute of Physiology, Russian Academy of Sciences, 6 Makarov Street, 199034 St. Petersburg, Russia.
Neurosci Behav Physiol. 2005 Jun;35(5):555-9. doi: 10.1007/s11055-005-0092-3.
The pathogenesis of migraine is based on the aseptic inflammation of dura mater tissues surrounding the large cranial vessels, such as the superior sagittal sinus. This inflammation develops in conditions of antidromic activation of sensory terminals of the trigeminal nerve and is accompanied by changes in the responses of neurons in the spinal nucleus of the trigeminal nerve to electrical stimulation of the superior sagittal sinus. However, the characteristics of the responses of these neurons to this stimulation have received virtually no study. Experiments on anesthetized rats were performed with recording of the responses of 387 neurons in the spinal nucleus of the trigeminal nerve to electrical stimulation of the superior sagittal sinus. The results showed that the responses of neurons to this stimulation was biphasic, consisting of a short initial phase with a latent period of 7-19 (11.4 +/- 0.17) msec, followed by a longer-lived discharge with a latent period of 20-50 (34.2 +/- 0.8) msec. It is suggested that the first phase reflects orthodromic activation of perivascular A(delta) and C fibers of the trigeminal nerve, while the second phase is associated with activation of meningeal C fibers with low conduction velocities and/or secondary activation of the perivascular sensory endings of the trigeminal nerve by algogenic and vasoactive substances released from them during antidromic activation. These changes seen in animal experiments may serve as an indicator of the efficacy of antimigraine agents.
