کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4327242 | 1614116 | 2010 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Diffuse traumatic brain injury initially attenuates and later expands activation of the rat somatosensory whisker circuit concomitant with neuroplastic responses
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کلمات کلیدی
IACUCTBIS1BFDAIGAP-43VPMAPPPBSqPCRNGScDNA - cDNAComplementary DNA - DNA تکمیلیFPI - REITTraumatic brain injury - آسیب تروماتیک مغزFluid percussion injury - آسیب سیاتیکDiffuse axonal injury - آسیب پذیری آسیب دیدهSport-Related Concussion - اختلالات مرتبط با ورزشRegeneration - باززاییInstitutional Animal Care and Use Committee - سازمان مراقبت و مراقبت از حیواناتnormal goat serum - سرم طبیعی بزPhosphate buffered saline - فسفات بافر شورBarrel field - میدان بشکهquantitative real-time polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی زمان واقعی استamyloid precursor protein - پروتئین پیش ماده آمیلوئی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Traumatic brain injury can initiate an array of chronic neurological deficits, effecting executive function, language and sensorimotor integration. Mechanical forces produce the diffuse pathology that disrupts neural circuit activation across vulnerable brain regions. The present manuscript explores the hypothesis that the extent of functional activation of brain-injured circuits is a consequence of initial disruption and consequent reorganization. In the rat, enduring sensory sensitivity to whisker stimulation directs regional analysis to the whisker barrel circuit. Adult, male rats were subjected to midline fluid percussion brain or sham injury and evaluated between 1 day and 42 days post-injury. Whisker somatosensory regions of the cortex and thalamus maintained cellular composition as visualized by Nissl stain. Within the first week post-injury, quantitatively less cFos activation was elicited by whisker stimulation, potentially due to axotomy within and surrounding the whisker circuit as visualized by amyloid precursor protein immunohistochemistry. Over six weeks post-injury, cFos activation after whisker stimulation showed a significant linear correlation with time in the cortex (r2 = 0.545; p = 0.015), non-significant correlation in the thalamus (r2 = 0.326) and U-shaped correlation in the dentate gyrus (r2 = 0.831), all eventually exceeding sham levels. Ongoing neuroplastic responses in the cortex are evidenced by accumulating growth associated protein and synaptophysin gene expression. In the thalamus, the delayed restoration of plasticity markers may explain the broad distribution of neuronal activation extending into the striatum and hippocampus with whisker stimulation. The sprouting of diffuse-injured circuits into diffuse-injured tissue likely establishes maladaptive circuits responsible for behavioral morbidity. Therapeutic interventions to promote adaptive circuit restructuring may mitigate post-traumatic morbidity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1323, 6 April 2010, Pages 161-173
Journal: Brain Research - Volume 1323, 6 April 2010, Pages 161-173
نویسندگان
Kelley D. Hall, Jonathan Lifshitz,