Srikiatkhachorn, Anan
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Preferred name
Srikiatkhachorn, Anan
Alternative Name
Srikiatkhachorn, Anon
Main Affiliation
Email
anan.sr@kmitl.ac.th
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Item type:Publication, Targeted orexin and hypothalamic neuropeptides for migraine(2018-02-13); Supronsinchai, WeeraThe hypothalamus is involved in the regulation of homeostatic mechanisms and migraine-related trigeminal nociception and as such has been hypothesized to play a central role in the migraine syndrome from the earliest stages of the attack. The hypothalamus hosts many key neuropeptide systems that have been postulated to play a role in this pathophysiology. Such neuropeptides include but are not exclusive too orexins, oxytocin, neuropeptide Y, and pituitary adenylate cyclase activating protein, which will be the focus of this review. Each of these peptides has its own unique physiological role and as such many preclinical studies have been conducted targeting these peptide systems with evidence supporting their role in migraine pathophysiology. Preclinical studies have also begun to explore potential therapeutic compounds targeting these systems with some success in all cases. Clinical efficacy of dual orexin receptor antagonists and intranasal oxytocin have been tested; however, both have yet to demonstrate clinical effect. Despite this, there were limitations in these cases and strong arguments can be made for the further development of intranasal oxytocin for migraine prophylaxis. Regarding neuropeptide Y, work has yet to begun in a clinical setting, and clinical trials for pituitary adenylate cyclase activating protein are just beginning to be established with much optimism. Regardless, it is becoming increasingly clear the prominent role that the hypothalamus and its peptide systems have in migraine pathophysiology. Much work is required to better understand this system and the early stages of the attack to develop more targeted and effective therapies aimed at reducing attack susceptibility with the potential to prevent the attack all together. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Migraine and its psychiatric comorbidities: The role of the amygdala(2018-01-01); Psychiatric comorbidities are common among patients with migraine. These comorbidities can compromise the quality of life of patients and may affect the result of treatment. The prevalence is higher in patients with migraine who overuse abortive medication. The mechanisms underlying these comorbidities remain unclear, but the amygdala is likely to be involved in their pathogenesis. This brain area has important functions in integrating sensory experiences with unpleasant emotions. The central amygdala plays a general integrative role in autonomic functions related to pain, and receives input from the outer layers of the trigeminal nucleus caudalis via the lateral parabrachial nucleus. A recent study showed that neurons in lateral parabrachial nucleus are activated more strongly by noxious stimulation of the face than of the hind paw. Increased excitability of laterocapsular division of the central nucleus of the amygdala has been observed in animals with cortical spreading depression, an electrophysiological phenomenon underlying the aura phase of migraine. Chronic treatment with analgesics further increases the neuronal excitability in the central nucleus of the amygdala and increases cortical spreading depression-evoked expression of Fos in the trigeminal nucleus caudalis and amygdala. These preclinical evidences imply the role of amygdala in pathogenesis of comorbid depression and anxiety commonly observed in patients with migraine. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, The potentiating effect of calcitonin gene-related peptide on transient receptor potential vanilloid-1 activity and the electrophysiological responses of rat trigeminal neurons to nociceptive stimuli(2018-05-01); Chetsawang, BanthitGrowing evidence suggests that calcitonin gene-related peptide (CGRP) participates in trigeminal nociceptive responses. However, the role of CGRP in sensitization or desensitization of nociceptive transduction remains poorly understood. In this study, we sought to further investigate the CGRP-induced up-regulation of transient receptor potential vanilloid-1 (TRPV1) and the responses of trigeminal neurons to nociceptive stimuli. Rat trigeminal ganglion (TG) organ cultures and isolated trigeminal neurons were incubated with CGRP. An increase in TRPV1 levels was observed in CGRP-incubated TG organ cultures. CGRP potentiated capsaicin-induced increase in phosphorylated CaMKII levels in the TG organ cultures. The incubation of the trigeminal neurons with CGRP significantly increased the inward currents in response to capsaicin challenge, and this effect was inhibited by co-incubation with the CGRP receptor antagonist, BIBN4068BS or the inhibitor of protein kinase A, H-89. These findings reveal that CGRP acting on trigeminal neurons may play a significant role in facilitating cellular events that contribute to the peripheral sensitization of the TG in nociceptive transmission. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Neural hyperactivity in the amygdala induced by chronic treatment of rats with analgesics may elucidate the mechanisms underlying psychiatric comorbidities associated with medication-overuse headache(2017-01-03) - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Altered activity in the nucleus raphe magnus underlies cortical hyperexcitability and facilitates trigeminal nociception in a rat model of medication overuse headache(2019-10-21); Supronsinchai, WeeraBackground : The pathogenesis of medication overuse headache (MOH) involves hyperexcitability of cortical and trigeminal neurons. Derangement of the brainstem modulating system, especially raphe nuclei may contribute to this hyperexcitability. The present study aimed to investigate the involvement of the nucleus raphe magnus (NRM) in the development of cortical and trigeminal hyperexcitability in a rat model of MOH. Results: Chronic treatment with acetaminophen increased the frequency of cortical spreading depression (CSD) and the number of c-Fos-immunoreactive (Fos-IR) neurons in the trigeminal nucleus caudalis (TNC). In the control group, muscimol microinjected into the NRM increased significantly the frequency of CSD-evoked direct current shift and Fos-IR neurons in the TNC. This facilitating effect was not found in rats with chronic acetaminophen exposure. In a model of migraine induced by intravenous systemic infusion of nitroglycerin (NTG), rats with chronic exposure to acetaminophen exhibited significantly more frequent neuronal firing in the TNC and greater Fos-IR than those without the acetaminophen treatment. Muscimol microinjection increased neuronal firing in the TNC in control rats, but not in acetaminophen-treated rats. The number of Fos-IR cells in TNC was not changed significantly. Conclusion: Chronic exposure to acetaminophen alters the function of the NRM contributing to cortical hyperexcitability and facilitating trigeminal nociception.