Srikiatkhachorn, Anan

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Srikiatkhachorn, Anan
Alternative Name
Srikiatkhachorn, Anon
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Email
anan.sr@kmitl.ac.th

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    Migraine and its psychiatric comorbidities: The role of the amygdala
    (2018-01-01)
    Wanasuntronwong, Aree
    ;
    Phiphopthatsanee, Nacharin
    ;
    Srikiatkhachorn, Anan
    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.
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    Nociceptive receptors are expressed differently in trigeminal nociception after lingual nerve injury and unilateral external carotid artery occlusion in rats
    (2021-06-01)
    Wanasuntronwong, Aree
    ;
    Punyawattananon, Visaluk
    ;
    Rotpenpian, Nattapon
    ;
    Meepong, Rittinarong
    ;
    Srikiatkhachorn, Anan
    Objectives: To investigate the different changes in nociceptive activity between two animal models of trigeminal neuropathic pain: unilateral external carotid artery ischemic reperfusion and lingual nerve crush in rats. Design: In this study, changes in nociceptive activity were investigated in unilateral external carotid artery ischemic reperfusion and lingual nerve crush models of trigeminal neuropathic pain in rats. Field excitatory postsynaptic potentials (fEPSPs) evoked by capsaicin application on the tongue of rats were recorded in the trigeminal nucleus caudalis. In addition, immunohistochemistry was performed in the trigeminal ganglia and trigeminal nucleus caudalis. Results: The fEPSP in unilateral external carotid artery ischemic reperfusion and lingual nerve crush rats was irregular relative to that in sham rats. In particular, the fEPSP spike in lingual nerve crush rats had a higher amplitude and shorter duration than that in sham rats. Unilateral external carotid artery ischemic reperfusion and lingual nerve crush also increased c-fos expression in the trigeminal nucleus caudalis. Upregulation of transient receptor potential vanilloid 1 in trigeminal ganglion was observed in unilateral external carotid artery ischemic reperfusion and lingual nerve crush rats, whereas upregulation of purinergic receptor subtype 3 in trigeminal ganglion was observed only in lingual nerve crush rats. Conclusions: Although unilateral external carotid artery ischemic reperfusion and lingual nerve crush similarly increased nociceptive activity at the trigeminal nucleus caudalis, the fEPSPs and expression of nociceptive peripheral afferent neurons were different. Therefore, direct and indirect nerve injuries apparently induced the same nociceptive activity by different signaling responses dependent on nociceptive receptors.
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    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)
    Wanasuntronwong, Aree
    ;
    Jansri, Ukkrit
    ;
    Srikiatkhachorn, Anan
    Background: Patients with medication-overuse headache suffer not only from chronic headache, but often from psychiatric comorbidities, such as anxiety and depression. The mechanisms underlying these comorbidities are unclear, but the amygdala is likely to be involved in their pathogenesis. To investigate the mechanisms underlying the comorbidities we used elevated plus maze and open field tests to assess anxiety-like behavior in rats chronically treated with analgesics. We measured the electrical properties of neurons in the amygdala, and examined the cortical spreading depression (CSD)-evoked expression of Fos in the trigeminal nucleus caudalis (TNC) and amygdala of rats chronically treated with analgesics. CSD, an analog of aura, evokes Fos expression in the TNC of rodents suggesting trigeminal nociception, considered to be a model of migraine. Results: Increased anxiety-like behavior was seen both in elevated plus maze and open field tests in a model of medication overuse produced in male rats by chronic treatment with aspirin or acetaminophen. The time spent in the open arms of the maze by aspirin- or acetaminophen-treated rats (53 ± 36.1 and 37 ± 29.5 s, respectively) was significantly shorter than that spent by saline-treated vehicle control rats (138 ± 22.6 s, P < 0.001). Chronic treatment with the analgesics increased the excitability of neurons in the central nucleus of the amygdala as indicated by their more negative threshold for action potential generation (-54.6 ± 5.01 mV for aspirin-treated, -55.2 ± 0.97 mV for acetaminophen-treated, and -31.50 ± 5.34 mV for saline-treated rats, P < 0.001). Chronic treatment with analgesics increased the CSD-evoked expression of Fos in the TNC and amygdala [18 ± 10.2 Fos-immunoreactive (IR) neurons per slide in the amygdala of rats treated with aspirin, 11 ± 5.4 IR neurons per slide in rats treated with acetaminophen, and 4 ± 3.7 IR neurons per slide in saline-treated control rats, P < 0.001]. Conclusions: Chronic treatment with analgesics can increase the excitability of neurons in the amygdala, which could underlie the anxiety seen in patients with medication-overuse headache.