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KMID : 1204320090250040317
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Laboratory Animal Research
2009 Volume.25 No. 4 p.317 ~ p.321
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Chronic Infusion of Sigma-1 Receptor Agonist Evokes Headache Symptom Through Brain-derived Neurotrophic Factor Activation in Rats
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Kim Kee-Won
Kwon Young-Bae
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Abstract
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Intracranial headaches are generally believed to be mediated by prolonged nociceptive activation of trigeminal nucleus caudalis (TNC) but the specific trigger factors are still poorly understood. Our accumulative studies demonstrate that sigma-1 receptors (Sig-1R) facilitate nociceptive transmission in the spinal cord. Based on these previous findings, the present study was conducted to further investigate whether chronic activation of Sig-1R could produce TNC neuronal activation as a key mechanism underlying the generation of headaches. Rats were intracisternally infused with the selective Sig-1R agonist PRE084 once or repeatedly for 14 day. A single infusion of PRE084 dose-dependently increased Fos like immunoreactive neurons (Fos-LI) in TNC without producing pain behavior (i.e. face grooming). Chronic infusion of PRE084 led to a comparable number of Fos-LI in TNC and similar pain behavior with that of the capsaicin single infusion, which is a commonly used headache model. Furthermore, PRE084 infusion for 14 days significantly increased the immunoreactivity of brain derived neurotrophic factor (BDNF) and its receptor tropomycin receptor kinase B in TNC. Thus, our findings indicate that the chronic activation of Sig-1R may evoke prolonged neuronal activation in the trigeminovascular system, which is related to the BDNF signaling pathway.
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KEYWORD
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Fos, headache, sigma-1 receptor, trigeminal nucleus caudalis, brain derived neurotrophic factor
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