کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6021968 | 1580660 | 2014 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differential trigeminovascular nociceptive responses in the thalamus in the familial hemiplegic migraine 1 knock-in mouse: A Fos protein study
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کلمات کلیدی
CGRPTrigeminovascularFHMCSDVPLVPMTCCTNCCACNA1Acortical spreading depression - افسردگی گسترش کورتکسAura - اوراtrigeminocervical complex - مجموعه سه گانه کرویMigraine - میگرنFamilial hemiplegic migraine - میگرن همی پلژی خانوادگیposterior thalamic nucleus - هسته تالامال خلفیtrigeminal nucleus caudalis - هسته سه هسته ای caudalisparafascicular thalamic nucleus - هسته ی تالامال پارافاسیکسیولارcalcitonin gene-related peptide - پپتید مرتبط با ژن کلسی تونین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Differential trigeminovascular nociceptive responses in the thalamus in the familial hemiplegic migraine 1 knock-in mouse: A Fos protein study Differential trigeminovascular nociceptive responses in the thalamus in the familial hemiplegic migraine 1 knock-in mouse: A Fos protein study](/preview/png/6021968.png)
چکیده انگلیسی
Familial hemiplegic migraine type 1 (FHM-1) is a monogenic subtype of migraine with aura caused by missense mutations in the CACNA1A gene, which encodes the pore-forming α1 subunit of voltage-gated neuronal CaV2.1 (P/Q-type) calcium channels. Transgenic knock-in mice expressing the CACNA1A R192Q mutation that causes FHM-1 in patients show a greater susceptibility to cortical spreading depression, the likely underlying mechanism of typical human migraine aura. The aim of this study was to compare neuronal activation within the trigeminal pain pathways in response to nociceptive trigeminovascular stimulation in wild-type and R192Q knock-in mice. After sham surgery or electrical stimulation of the superior sagittal sinus for 2 h, or stimulation preceded by treatment with naratriptan, mice underwent intracardiac perfusion, and the brain, including the brainstem, was removed. Fos expression was measured in the trigeminocervical complex (TCC) and the lateral (ventroposteromedial, ventrolateral), medial (parafascicular, centromedian) and posterior thalamic nuclei. In the TCC of wild-type animals, the number of Fos-positive cells increased significantly following dural stimulation compared to the sham control group (P < 0.001) and decreased after naratriptan treatment (P < 0.05). In R192Q knock-in mice, there was no significant difference between the stimulated and sham (P = 0.10) or naratriptan pre-treated groups (P = 0.15). The number of Fos-positive cells in the R192Q stimulated group was significantly lower compared to the wild-type stimulated mice (P < 0.05). In the thalamus, R192Q mice tended to be more sensitive to stimulation compared to the sham control in the medial and posterior nuclei, and between the two strains of stimulated animals there was a significant difference in the centromedian (P < 0.005), and posterior nuclei (P < 0.05). The present study suggests that the FHM-1 mutation affects more rostral brain structures in this experimental paradigm, which offers a novel perspective on possible differential effects of mutations causing migraine in terms of phenotype-genotype correlations.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 64, April 2014, Pages 1-7
Journal: Neurobiology of Disease - Volume 64, April 2014, Pages 1-7
نویسندگان
JungWook Park, HeuiSoo Moon, Simon Akerman, Philip R. Holland, Michele P. Lasalandra, Anna P. Andreou, Michel D. Ferrari, Arn M.J.M. van den Maagdenberg, Peter J. Goadsby,