Abstract:
Migraine headache generates in trigeminal nociceptive system which is activated by cortical spreading depression (CSD) phenomenon. There are also some neurotransmitter changes relating to pathogenesis of migraine, one of representative examples is serotonin (5-HT) depletion that may predispose to migraine development. Trigeminal ganglion (TG) is a structure containing cell body of neurons that undertakes a role as first order neuron in trigeminal nociceptive system. Moreover, the alteration of glutamate may contribute to hyperactivity of its specific receptors, for instance N-methyl-D-aspartate (NMDA) receptor. Endogenous biomolecule, such as kynurenic acid (KYNA) which is derived form of 5-HT can inhibit NMDA receptor. Basically, KYNA plays a role as NMDA antagonist, and at the same time, it is one of metabolites of tryptophan pathways as well as 5-HT. This study aimed to explore the electrophysiological properties change of TG neuron isolated from rat migraine models (CSD and 5-HT depletion), and the effects of KYNA on them. The results revealed that resting membrane potential (RMP) of TG neurons had significant depolarization shift in CSD and combined model of CSD and 5-HT depletion, while this alteration was not observed in 5-HT depletion only. In conclusion, CSD is a cortical model of migraine that affects to TG neuron. Thus, CSD has a potential to alter RMP of TG neurons that may results to increase of neuronal excitability in trigeminal nociceptive system.
