Effects of Sumatriptan on PACAP, PAC-1, CGRP, VIP, and TRPV-1 Molecules in an Experimental Migraine Model

Abstract Migraine is a chronic neurological disorder characterized by severe headache. In the pathology of migraine, it is suggested that increased parasympathetic output to intracranial arteries due to excessive stimulation of the trigeminovascular system is responsible. The release of PACAP, VIP, and CGRP signaling molecules due to excessive stimulation leads to the dilation of intracranial arteries, causing headaches. Sumatriptan exerts its therapeutic effect by causing vasoconstriction of dilated meningeal blood vessels in migraine and suppressing the release of vasoactive neuropeptides from trigeminal sensory neurons. However, the relationship between the Sumatriptan and the signaling pathways in migraine pathology has not been sufficiently studied. In this study, we aimed to determine the potential therapeutic efficacy of the Sumatriptan on PACAP, PAC-1, CGRP, VIP, and TRPV1 molecules in an experimental migraine model. In the study, 62 Sprague Dawley rats (31 males and 31 females) weighing 250–300 g were randomly divided into five experimental groups: Control, Sham, Migraine, Sumatriptan, and Migraine-Sumatriptan, with procedures followed accordingly, with Sumatriptan administered as a 14-day chronic treatment regimen. At the end of the study, histopathological evaluation of brain tissues taken from the animals was performed, and the immunoreactivity of PACAP, PAC-1, CGRP, VIP, and TRPV1 proteins was assessed immunohistochemically. As a result, it was observed that the histopathological findings were observed to decrease in the migraine group treated with sumatriptan compared to the migraine group ( p < 0.0001). Based on the obtained data, it was determined that sumatriptan significantly affected the neuropeptides associated with pain in migraine. However, more detailed analyses are still needed in this regard.