Journal
MOLECULAR NEUROBIOLOGY
Volume 58, Issue 11, Pages 5581-5601Publisher
SPRINGER
DOI: 10.1007/s12035-021-02503-w
Keywords
Apoptosis; Migraine; Oxidative stress; PARP1; Trigeminal ganglia; TRPM2 channel
Categories
Funding
- Scientific Research Project Unit (BAP), Suleyman Demirel University, Isparta, Turkey [TDK-2020-7448]
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The activation and maintenance of TRPM2 channel play critical roles in regulating pain, oxidative stress, apoptosis, inflammation, and other processes involved in migraine. Activation of TRPM2 can further increase pain and cell damage induced by glyceryl trinitrate, while restoring the balance of TRPM2 channels helps alleviate these discomforts.
Excessive Ca2+ influx and mitochondrial oxidative stress (OS) of trigeminal ganglia (TG) have essential roles in the etiology of migraine headache and aura. The stimulation of TRPM2 channel via the generation of OS and ADP-ribose (ADPR) induces pain, inflammatory, and oxidative neurotoxicity, although its inhibition reduces the intensity of pain and neurotoxicity in several neurons. However, the cellular and molecular effects of TRPM2 in the TG of migraine model (glyceryl trinitrate, GTN) on the induction of pain, OS, apoptosis, and inflammation remain elusive. GTN-mediated increases of pain intensity, apoptosis, death, cytosolic reactive oxygen species (ROS), mitochondrial ROS, caspase -3, caspase -9, cytosolic Ca2+ levels, and cytokine generations (TNF-alpha, IL-1 beta, and IL-6) in the TG of TRPM2 wild-type mouse were further increased by the TRPM2 activation, although they were modulated by the treatments of GSH, PARP-1 inhibitors (PJ34 and DPQ), and TRPM2 blockers (ACA and 2APB). However, the effects of GTN were not observed in the TG of TRPM2 knockout mice. The current data indicate that the maintaining activation of TRPM2 is not only important for the quenching OS, inflammation, and neurotoxicity in the TG neurons of mice with experimental migraine but also equally critical to the modulation of GTN-induced pain.
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