Bu çalışmada hibe Ulusal Araştırma Vakfı (NMK-2014R1A2A1A11052042; 2015M3A9B4067068), Bilim Bakanlığı ve teknoloji, Kore, Kore sağlık teknoloji R & D Projesi (HI16C1012), Sağlık Bakanlığı tarafından desteklenen & Refah, Kore ve "Dongwha" fakülte araştırma yardım programı Yonsei Üniversitesi College of Medicine (6-2016-0126).

Bütün hayvanlar standart bir kafeste (27 x 22,5 × 14 cm3) değerlendirme ve Akreditasyon, laboratuvar hayvan bakım (AAALAC) Derneği tarafından akredite edilmiş ve yiyecek verilen bir tesiste yer alan ve 12-h açık/koyu alternatif altında ad libitum su geçiş yapar. Yazarlar hayvan koruma hükümlerine takip ve deneysel prosedürler kurumsal hayvan bakım ve kullanım Komitesi Yonsei Üniversitesi Üniversite Tıp tarafından kabul edildi (IACUC No 2010-0252; 2013-0220).
1. fare modeli yenidoğan HI beyin hasarı
<ol><li>Belgili tanımlık pups isoflurane ile anestezi.<ol>
<li>Belgili tanımlık pups (daha az 5) anesthetizing bir kutuya yerleştirin ve kapağını kapatın.</li>
		<li>Yaklaşık 15 dakika anesthetizing sistem açın; gaz ve tablo üst anestezi makinasıyla isoflurane ayarlayın. 1, 5 L/dak ayarlama isoflurane Buharlaştırıcı anestezi indüksiyon için 3-%5 için oksijen Flowmetre ayarlayın.</li>
		<li>15 dk sonra isoflurane Buharlaştırıcı anestezi bakımı için 1-%2 için ayarlayın.</li>
	</ol>
</li>
	<li>Tam imzalat bir yavru bir diseksiyon mikroskop (araştırmacı karşı karşıya karin) altında yatıyordu ve bant ile sabitleyin.</li>
	<li>Bir ~0.7-mm kesi sterilize makas kullanarak boynundan olun.</li>
	<li>Dikkatle sterilize forseps kullanarak yağ dokusu kaldırmak ve tek taraflı şu Şah damarı açığa.</li>
	<li>5-0 absorbe dikiş ile tek taraflı sağ Karotis arter ligate.</li>
	<li>Kesik boyun ile 5-0 Dikiş dikiş.</li>
	<li>Her yavru için kurtarma için 1 h 37 ° C sıcak hipoksik odası yerleştirin. Odası kapağını kapatmayın.</li>
	<li>Ameliyattan sonra 1 h ne zaman belgili tanımlık pups tamamen uyanık, hipoksi odası kapağını kapatın ve hipoksik koşullarını (%8 O2 , %92 N2) oluşturmak için gaz seviyesi azaltın.</li>
	<li>Hipoksi, 90 dakika sonra yavrular için onların kafes dönmek.</li>
	<li>Bir hafta sonra HI beyin hasarı, 1. adımı yineleyin.<ol>
<li>Anestezi sonra bir kesi ile sterilize makas ve forseps beyin lezyon sağ hemisfer posterolateral alanında tanımlamak için kafa derisi içinde olun. Not: Bu tedavi hipoksi pups içinde neden olmaktadır. Varlığı ve tüm farelerde beyin hasarının ölçüde görsel olarak değerlendirildi yarı saydam kafatası ile çıplak gözle. Boyut veya renk değişikliği (yani, beyin lezyon) hacmi tarafından belirlenen pups gruplar halinde sınıflandırılır. Hiçbir görünür kortikal yaralanma varsa, fare "hiçbir kortikal yaralanma" grup olarak sınıflandırılır. Görünür bir kortikal yaralanma (yani, bir lezyon sağ hemisfer) ise, fare "kortikal yaralanma" grup olarak sınıflandırılır. Fareler sınıflandırılması gruplar halinde ameliyat sonrası bir hafta beri beyin örnekleri türleri Morfoloji açıkça kurban1,2,3sırada tanımlanır gruplandırmalar değiştirilebilir, 4.</li>
	</ol>
</li>
</ol><img alt="Figure 1" class="xfigimg" src="/files/ftp_upload/55838/55838fig1v3.jpg"> Resim 1: farelerde neonatal HI beyin hasarı modelleme. (A) bir yedi günlük eski fare yavru ameliyat oldu ve tek taraflı şu Karotid arter bakmaksızın. (B) pups hipoksik Odası %8 O2 ve % 92 N290 dk için yerleştirildi. (C, D ve E) Yenidoğan HI yaralanma ile beyin hasar çeşitli önem gösterdi ve hasarı derecesine göre kategorize edildi. Haftası 14, beyin elde edilmiştir ve bu lezyonlar görüntülenir. (C) bir "hiçbir kortikal yaralanma" gizli bir beyin görüntüsünü. Her iki (D) ve (E) "kortikal yaralanma" grup olarak sınıflandırıldı. (F, G ve H) Temsilcisi MRI (c), (D) ve (E) fareler, anılan sıraya göre. (F) hasar oluşur içinde sarı bir ok ile gösterilir ve sağ hemisfer lezyonlarının da sarı oklarla (G ve H) gösterilir. Ölçek çubukları = 1 mm <a href="http://cloudflare.jove.com/files/ftp_upload/55838/55838fig1v3large.jpg" target="_blank">Bu rakam daha büyük bir versiyonunu görüntülemek için buraya tıklayınız.</a>
2. yenidoğan davranış testleri
Not: Burada, 6 haftalık davranış testleri yapıldı.
<ol><li>
Pasif kaçınma görev. Not: bellek işlevi öğrenme ve caydırıcı bir uyarıcı kaçınma dayalı değerlendirmek için adım aracılığıyla bir iki bölmeli PAT yapılan13,14,15,16olması gerekir.<ol>
<li>Bir fare bir PAT aparatı pleksiglas Servisi kutusunu (41,5 × 21 × 35 cm3) parlak bölmesine yerleştirin.</li>
		<li>Sonra 30 s, giyotin kapı açık ve koyu bölmesine taşımak fare gecikme süresi saatlerini kaydetmek (300 s).</li>
		<li>Fare tüm dört bacaklarda tam içinde karanlık bölme olduğunda Giyotin kapıyı kapat.</li>
		<li>Elektrikli ayak şok yönetmek (0,5 mA) 2 s ve onun kafes fare dönmek için.</li>
		<li>Fareyi parlak yerde 24 saat elektrik ayak şoktan sonra değiştirin.</li>
		<li>Fare tamamen parlak kompartımanda yerleştirildikten sonra Giyotin kapı 10 s açın ve karanlık bölmesine taşımak fare gecikme süresi saatlerini kaydetmek (300 s).</li>
	</ol>
</li>
	<li>
Merdiven yürüme testi. Not: Merdiven basamak yürüyen görev ince bozuklukları motor işlevleri birleştirerek nitel ve nicel analizler yetenekli yürüyen17,18arasında ayrımcılık için izin verir.<ol>
<li>Bir video kamerayı açın.</li>
		<li>Bir fare merdiven başlangıç paneli üzerindeki yeri ve hemen kayıt başlar.</li>
		<li>Fare bacaklarda üzerinde odaklanan video kaydetmek.</li>
		<li>Fare merdivenin son paneli dokunduğunda kaydı durdur. İleri geri seyahat dört kere tekrar edin.</li>
		<li>Video kaydı analiz ve el ile her forelimb notları aşağıdaki gibi sayma:<ol>
<li>Bir bilgisayar yavaş hızda video kaydı Çal (0.1 x) ve adımları el ile saymak.</li>
		</ol>
</li>
	</ol>
</li>
	<li>
Kavrama gücü test. Not: Kavrama gücü test bir itme-çekme ağırlık ölçme esneklik detektörler içerir bir kavrama gücü ölçer kullanılarak gerçekleştirilir.<ol>
<li>Kavrama gücü aparatı akrilik bir panel üzerine düzeltmek.</li>
		<li>Akrilik panelde yer bir fare ve onun kuyruk tutun.<ol>
<li>Fare erişebilmesi kuyruğunu tutan el ve kavrama cihazları metal tel taşıyın.</li>
		</ol>
</li>
		<li>Fareyi bir üçgen parça metal tel (2 mm çapında); kulpları kadar birden fazla deneme izin tepe Kuvvetleri gram cihaz tarafından otomatik olarak kaydedilir. Not: ortalama en yüksek güç üç denemeler analiz19,20,21için kullan.</li>
	</ol>
</li>
</ol>

<ol>
	<li>Yager, J. Y. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Animal+models+of+hypoxic-ischemic+brain+damage+in+the+newborn.">Animal models of hypoxic-ischemic brain damage in the newborn.</a> Semin Pediatr Neurol. 11 (1), 31-46 (2004).</li><li>Vannucci, R. C., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Rat+model+of+perinatal+hypoxic-ischemic+brain+damage.">Rat model of perinatal hypoxic-ischemic brain damage.</a> J Neurosci Res. 55 (2), 158-163 (1999).</li><li>Im, S. H., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Induction+of+striatal+neurogenesis+enhances+functional+recovery+in+an+adult+animal+model+of+neonatal+hypoxic-ischemic+brain+injury.">Induction of striatal neurogenesis enhances functional recovery in an adult animal model of neonatal hypoxic-ischemic brain injury.</a> Neuroscience. 169 (1), 259-268 (2010).</li><li>Clowry, G. J., Basuodan, R., Chan, F. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=What+are+the+Best+Animal+Models+for+Testing+Early+Intervention+in+Cerebral+Palsy?.">What are the Best Animal Models for Testing Early Intervention in Cerebral Palsy?.</a> Front Neurol. 5 (258), 1-17 (2014).</li><li>Colver, A., Fairhurst, C., Pharoah, P. O. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Cerebral+palsy.">Cerebral palsy.</a> Lancet. 383 (9924), 1240-1249 (2014).</li><li>Levine, S. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Anoxic-ischemic+encephalopathy+in+rats.">Anoxic-ischemic encephalopathy in rats.</a> Am J Pathol. 36, 1-17 (1960).</li><li>Rice 3rd, J. E., Vannucci, R. C., Brierley, J. B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+influence+of+immaturity+on+hypoxic-ischemic+brain+damage+in+the+rat.">The influence of immaturity on hypoxic-ischemic brain damage in the rat.</a> Ann Neurol. 9 (2), 131-141 (1981).</li><li>Lafemina, M. J., Sheldon, R. A., Ferriero, D. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Acute+hypoxia-ischemia+results+in+hydrogen+peroxide+accumulation+in+neonatal+but+not+adult+mouse+brain.">Acute hypoxia-ischemia results in hydrogen peroxide accumulation in neonatal but not adult mouse brain.</a> Pediatr Res. 59 (5), 680-683 (2006).</li><li>Brazel, C. Y., Rosti 3rd, R. T., Boyce, S., Rothstein, R. P., Levison, S. W. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Perinatal+hypoxia/ischemia+damages+and+depletes+progenitors+from+the+mouse+subventricular+zone.">Perinatal hypoxia/ischemia damages and depletes progenitors from the mouse subventricular zone.</a> Dev Neurosci. 26 (2-4), 266-274 (2004).</li><li>Buono, K. D., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Mechanisms+of+mouse+neural+precursor+expansion+after+neonatal+hypoxia-ischemia.">Mechanisms of mouse neural precursor expansion after neonatal hypoxia-ischemia.</a> J Neurosci. 35 (23), 8855-8865 (2015).</li><li>Rumajogee, P., Bregman, T., Miller, S. P., Yager, J. Y., Fehlings, M. G. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Rodent+Hypoxia-Ischemia+Models+for+Cerebral+Palsy+Research:+A+Systematic+Review.">Rodent Hypoxia-Ischemia Models for Cerebral Palsy Research: A Systematic Review.</a> Front Neurol. 7 (57), 1-20 (2016).</li><li>Hagberg, H., Peebles, D., Mallard, C. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Models+of+white+matter+injury:+comparison+of+infectious,+hypoxic-ischemic,+and+excitotoxic+insults.">Models of white matter injury: comparison of infectious, hypoxic-ischemic, and excitotoxic insults.</a> Ment Retard Dev Disabil Res Rev. 8 (1), 30-38 (2002).</li><li>Wi, S., Yu, J. H., Kim, M., Cho, S. R. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=In+Vivo+Expression+of+Reprogramming+Factors+Increases+Hippocampal+Neurogenesis+and+Synaptic+Plasticity+in+Chronic+Hypoxic-Ischemic+Brain+Injury.">In Vivo Expression of Reprogramming Factors Increases Hippocampal Neurogenesis and Synaptic Plasticity in Chronic Hypoxic-Ischemic Brain Injury.</a> Neural Plast. 2016 (2580837), 1-11 (2016).</li><li>Lu, Y., Christian, K., Lu, B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=BDNF:+a+key+regulator+for+protein+synthesis-dependent+LTP+and+long-term+memory?.">BDNF: a key regulator for protein synthesis-dependent LTP and long-term memory?.</a> Neurobiol Learn Mem. 89 (3), 312-323 (2008).</li><li>Manabe, T., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Facilitation+of+long-term+potentiation+and+memory+in+mice+lacking+nociceptin+receptors.">Facilitation of long-term potentiation and memory in mice lacking nociceptin receptors.</a> Nature. 394 (6693), 577-581 (1998).</li><li>Alonso, M., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=BDNF-triggered+events+in+the+rat+hippocampus+are+required+for+both+short-+and+long-term+memory+formation.">BDNF-triggered events in the rat hippocampus are required for both short- and long-term memory formation.</a> Hippocampus. 12 (4), 551-560 (2002).</li><li>Seo, J. H., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=In+Situ+Pluripotency+Factor+Expression+Promotes+Functional+Recovery+From+Cerebral+Ischemia.">In Situ Pluripotency Factor Expression Promotes Functional Recovery From Cerebral Ischemia.</a> Mol Ther. 24 (9), 1538-1549 (2016).</li><li>Kim, M. S., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Environmental+enrichment+enhances+synaptic+plasticity+by+internalization+of+striatal+dopamine+transporters.">Environmental enrichment enhances synaptic plasticity by internalization of striatal dopamine transporters.</a> J Cereb Blood Flow Metab. 36 (12), 2122-2133 (2015).</li><li>Lee, M. Y., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Alteration+of+synaptic+activity-regulating+genes+underlying+functional+improvement+by+long-term+exposure+to+an+enriched+environment+in+the+adult+brain.">Alteration of synaptic activity-regulating genes underlying functional improvement by long-term exposure to an enriched environment in the adult brain.</a> Neurorehabil Neural Repair. 27 (6), 561-574 (2013).</li><li>Rha, D. W., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Effects+of+constraint-induced+movement+therapy+on+neurogenesis+and+functional+recovery+after+early+hypoxic-ischemic+injury+in+mice.">Effects of constraint-induced movement therapy on neurogenesis and functional recovery after early hypoxic-ischemic injury in mice.</a> Dev Med Child Neurol. 53 (4), 327-333 (2011).</li><li>Chong, H. J., Cho, S. R., Jeong, E., Kim, S. J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Finger+exercise+with+keyboard+playing+in+adults+with+cerebral+palsy:+A+preliminary+study.">Finger exercise with keyboard playing in adults with cerebral palsy: A preliminary study.</a> J Exerc Rehabil. 9 (4), 420-425 (2013).</li><li>Chong, H. J., Cho, S. R., Kim, S. J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Hand+rehabilitation+using+MIDI+keyboard+playing+in+adolescents+with+brain+damage:+a+preliminary+study.">Hand rehabilitation using MIDI keyboard playing in adolescents with brain damage: a preliminary study.</a> NeuroRehabilitation. 34 (1), 147-155 (2014).</li><li>Seo, J. H., Yu, J. H., Suh, H., Kim, M. S., Cho, S. R. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Fibroblast+growth+factor-2+induced+by+enriched+environment+enhances+angiogenesis+and+motor+function+in+chronic+hypoxic-ischemic+brain+injury.">Fibroblast growth factor-2 induced by enriched environment enhances angiogenesis and motor function in chronic hypoxic-ischemic brain injury.</a> PLoS One. 8 (9), e74405 (2013).</li><li>Washington, P. M., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+effect+of+injury+severity+on+behavior:+a+phenotypic+study+of+cognitive+and+emotional+deficits+after+mild,+moderate,+and+severe+controlled+cortical+impact+injury+in+mice.">The effect of injury severity on behavior: a phenotypic study of cognitive and emotional deficits after mild, moderate, and severe controlled cortical impact injury in mice.</a> J Neurotrauma. 29 (13), 2283-2296 (2012).</li><li>Cho, S. R., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Astroglial+Activation+by+an+Enriched+Environment+after+Transplantation+of+Mesenchymal+Stem+Cells+Enhances+Angiogenesis+after+Hypoxic-Ischemic+Brain+Injury.">Astroglial Activation by an Enriched Environment after Transplantation of Mesenchymal Stem Cells Enhances Angiogenesis after Hypoxic-Ischemic Brain Injury.</a> Int J Mol Sci. 17 (9), 1-15 (2016).</li><li>Tsuji, M., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=A+novel+reproducible+model+of+neonatal+stroke+in+mice:+comparison+with+a+hypoxia-ischemia+model.">A novel reproducible model of neonatal stroke in mice: comparison with a hypoxia-ischemia model.</a> Exp Neurol. 247, 218-225 (2013).</li></ol>

Yazarlar hiçbir rakip ilgi alanlarına sahip.

Bu çalışmada biz HI beyin hasarı yenidoğan P7-10 CD-1 Mouse indüklenen ve beyin lezyon ile ilgili motor ve Bilişsel açıkları tespit. Bu işlem sırasında tek taraflı şu Karotid arter tıkanıklığı son derece önemliydi. Bu adımda, arter zarar görmüş ve yırtılmış. Çoğu yavru bir arter gözyaşı deneyimli öldü. Tersine, araştırmacılar tek taraflı şu Karotid arter yerine başka bir kan damarı bakmaksızın, yavru fok beyin sadece hafif hasar gördü ve hiçbir önemli fenotip<sup class="xr...

Yenidoğan HI beyin hasarı erken çocukluk (yaklaşık 1000 çocuk başına iki hasta)1,2,3,4,5sırasında oluşur. Yenidoğan HI beyin hasarı ile ilgili çalışmalar, ve önemli bir kurulan yenidoğan HI beyin yaralanması fare modeli kullanarak HI beyin hasarı in vivo preklinik araştırma kolaylaştırabilir.
Geleneksel HI modelleri üzerinde yetişkin fareler6kullanılır. Kardiyolojik modeli için pirinç-Vannucci yöntemi P7 fareler7,8yaygın olarak kullanılır. Sıçanlar ve fareler her iki kemirgen olsa bile biraz farklı9,10, olduğundan Ancak, biz bir değiştirilmiş pirinç-Vannucci yöntemi üzerinde CD-1 pups P7-10, tabanlı P7-10 dönemi olduğunu gösterdi önceki çalışmaları üzerinde gerçekleştirilen featuring olgunlaşmamış oligodendrocytes, insan terim P011,12karşılık gelen. Yenidoğan HI fare modeli P7-10 pups içinde tek taraflı Karotid arter her iki tüp ligasyonu ve fareler maruz hipoksi %8 oksijen ile kurulur.
Fareyi sağ hemisfer posterolateral alanında değişik derecelerde beyin lezyonları gösterdi yordamı tabi. Bilişsel ve motor açıkları, neurobehavioral değerlendirmeler üzerinde PAT dayalı tanımlamak için test ve kavrama gücü testi yürüyen merdiven yapıldı. Sigara işletilen (Yani, normal) ve HI fareler arasındaki farkları analiz edildi. Bu eser HI fare modeli hakkında temel bilgi sunar. MRI görüntüleri beyin hasar motor ve Bilişsel testleri kullanarak şiddetine göre ayrılmış farklı fenotipleri göstermektedir.

<table border="0" cellpadding="0" cellspacing="0" width="1008">
	<tbody>
		<tr height="25">
			<td height="25" style="height:25px;width:363px;">Hypoxic chamber</td>
			<td style="width:203px;">Jeung Do Bio &#38; Plant Co</td>
			<td colspan="2" style="width:443px;">Experimental Builder&#160;</td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;">PAT apparatus&#160;</td>
			<td>Jeung Do Bio &#38; Plant Co</td>
			<td colspan="2">Experimental Builder&#160;</td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;">The ladder rung walking&#160;</td>
			<td>Jeung Do Bio &#38; Plant Co</td>
			<td colspan="2">Experimental Builder&#160;</td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;">SDI Grip Strength System&#160;</td>
			<td colspan="2">San Diego Instruments Inc.</td>
			<td></td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;width:363px;">Grip-Strength Meter</td>
			<td>Ugo Basile&#160;</td>
			<td align="right">47200</td>
			<td></td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;">Harvard Apparatus Fluovac anesthetizing system&#160;</td>
			<td>Harvard Apparatus</td>
			<td></td>
			<td></td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;">Anesthetizing box</td>
			<td></td>
			<td></td>
			<td>acryl box</td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;">I-Fran Liquid (Isofluorane)</td>
			<td>Hana Pharm. Co., Ltd.</td>
			<td></td>
			<td>General Anesthetics ( isoflurane 100ml)</td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;">CD-1 mice</td>
			<td>Orient Co., Ltd.</td>
			<td></td>
			<td></td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;">Blue Nylon Mono Non-Absorbbable suture 5-0 50cm</td>
			<td>Ailee Co., Ltd.</td>
			<td>NB 521</td>
			<td></td>
		</tr>
		<tr height="25">
			<td height="25" style="height:25px;">IBM SPSS Statistics</td>
			<td>IBM</td>
			<td>Ver. 23</td>
			<td></td>
		</tr>
	</tbody>
</table>

neurobehavioral assessments in a mouse model of neonatal hypoxic-ischemic brain injury

Biz tek taraflı Karotis arter tıkanıklığı bir yenidoğan hipoksik-iskemik (hı) model oluşturmak için CD-1 fareler üzerinde gerçekleştirilen ve neurobehavioral işlevleri olmayan işletilen (Yani, için karşılaştırıldığında bu farelerde inceleyerek yenidoğan HI beyin hasarı etkileri araştırıldı Normal) fareler. Çalışma sırasında pirinç-Vannucci'nın yöntemi postnatal gün 7-10 (P7-10) farelerde neonatal HI beyin hasar ikna etmek için kullanıldı. HI işlem üzerinde belgili tanımlık pups tek taraflı Karotis arter ligasyonu ve hipoksi (%8 O2 ve %92 N2 90 dk) maruz tarafından gerçekleştirildi. Bir hafta sonra ameliyat, hasarlı beyin yarı saydam kafatası ile çıplak gözle değerlendirildi ve devamsızlık ("hiçbir kortikal yaralanma" grubu) veya kortikal yaralanma ("kortikal yaralanma" grubu) varlığı göre alt gruplar halinde kategorize, sağ hemisfer bir lezyon gibi. 6 haftasında bilişsel ve motor işlevlerinin değerlendirmek için aşağıdaki neurobehavioral testler gerçekleştirilmiştir: pasif kaçınma görev (PAT), merdiven test ve kavrama gücü testi yürüme. Bu davranış testleri yenidoğan HI beyin hasarının etkilerini belirlemede yararlı ve nörodejeneratif hastalıklar diğer fare modellerinde kullanılır. Bu çalışmada yenidoğan HI beyin yaralanması fare Sağ Yarımküre hasar denk motor açıkları gösterdi. Davranışsal test sonuçlarını beyin felci veya neonatal inme hastalarında gibi insan yenidoğan HI hastalarda gözlenen açıkları alakalı. Bu çalışmada yenidoğan HI beyin hasarı bir fare modeli kurulan ve motor açıkları ve kognitif bozukluk sigara çalışan fareler için karşılaştırıldığında farklı derecelerde gösterdi. Bu eser HI fare modeli üzerinde temel bilgileri sağlar. MRI görüntüleri beyin hasarı şiddetine göre motor ve Bilişsel testleri tarafından ayrılmış farklı fenotipleri göstermektedir.

Tüm veriler ortalama ± standart hata ortalamaya (SEM) ifade edilir. Değişkenleri iki grup arasında karşılaştırma bağımsız veya eşleştirilmiş tkullanılarak yapılmıştır-testi SPSS istatistik yazılımı. Bir p-değeri < 0,05 olarak istatistiksel olarak anlamlı kabul.
Yenidoğan HI yaralanma ile beyin hasar farklı önem gösterdi ve buna göre kategorize edildi (şekil 1 ...

Watch this Scientific Journal Video about Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury at JoVE.com

Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury

Tek taraflı Karotis arter tıkanıklığı postnatal gününde gerçekleştirilen 7-10 CD-1 fare pups yenidoğan hipoksik-iskemik (hı) model oluşturmak ve HI beyin hasarı etkileri araştırıldı. Neurobehavioral işlevleri olmayan çalışan normal farelere göre bu farelerde görmüştük.

Yenidoğan hipoksik-iskemik beyin hasarı, fare modeli neurobehavioral değerlendirmesi

We performed unilateral carotid artery occlusion on CD-1 mice to create a neonatal hypoxic-ischemic (HI) model and investigated the effects of neonatal HI ...

neurobehavioral-assessments-mouse-model-neonatal-hypoxic-ischemic

Research

JoVE Journal

Neuroscience

12.2K Görüntüleme.  Yonsei University College of Medicine. Tek taraflı Karotis arter tıkanıklığı postnatal gününde gerçekleştirilen 7-10 CD-1 fare pups yenidoğan hipoksik-iskemik (hı) model oluşturmak ve HI beyin hasarı etkileri araştırıldı. Neurobehavioral işlevleri olmayan çalışan normal farelere göre bu farelerde görmüştük.

Video: Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury

Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice

Traumatic brain injury (TBI) research has attained renewed momentum due to the increasing awareness of head injuries, which result in morbidity and mortality. Based on the nature of primary injury following TBI, complex and heterogeneous secondary consequences result, which are followed by regenerative processes 1,2. Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement 3,4. The resulting hematomas and lacerations cause a vascular response 3,5, and the morphological and functional damage of the white matter leads to diffuse axonal injury 6-8. Additional secondary changes commonly seen in the brain are edema and increased intracranial pressure 9. Following TBI there are microscopic alterations in biochemical and physiological pathways involving the release of excitotoxic neurotransmitters, immune mediators and oxygen radicals 10-12, which ultimately result in long-term neurological disabilities 13,14. Thus choosing appropriate animal models of TBI that present similar cellular and molecular events in human and rodent TBI is critical for studying the mechanisms underlying injury and repair.
Various experimental models of TBI have been developed to reproduce aspects of TBI observed in humans, among them three specific models are widely adapted for rodents: fluid percussion, cortical impact and weight drop/impact acceleration 1. The fluid percussion device produces an injury through a craniectomy by applying a brief fluid pressure pulse on to the intact dura. The pulse is created by a pendulum striking the piston of a reservoir of fluid. The percussion produces brief displacement and deformation of neural tissue 1,15. Conversely, cortical impact injury delivers mechanical energy to the intact dura via a rigid impactor under pneumatic pressure 16,17. The weight drop/impact model is characterized by the fall of a rod with a specific mass on the closed skull 18. Among the TBI models, LFP is the most established and commonly used model to evaluate mixed focal and diffuse brain injury 19. It is reproducible and is standardized to allow for the manipulation of injury parameters. LFP recapitulates injuries observed in humans, thus rendering it clinically relevant, and allows for exploration of novel therapeutics for clinical translation 20.
We describe the detailed protocol to perform LFP procedure in mice. The injury inflicted is mild to moderate, with brain regions such as cortex, hippocampus and corpus callosum being most vulnerable. Hippocampal and motor learning tasks are explored following LFP.

Lateral fluid percussion (LFP), an established model of traumatic brain injury in mice, is demonstrated. LFP fulfills three major criteria for animal models: validity, reliability and clinical relevance. The procedure, consisting of surgical craniotomy, fixation of hub followed by induction of injury, resulting in focal and diffuse injuries, is described.

Yanal Akışkan Perküsyon: Travmatik Beyin Hasarı Farelerde Modeli

Traumatic brain injury (TBI) research has attained renewed momentum due to the increasing awareness of head injuries, which result in morbidity and ...

Nörobilim

Intracerebroventricular Viral Injection of the Neonatal Mouse Brain for Persistent and Widespread Neuronal Transduction

With the pace of scientific advancement accelerating rapidly, new methods are needed for experimental neuroscience to quickly and easily manipulate gene expression in the mouse brain. Here we describe a technique first introduced by Passini and Wolfe for direct intracranial delivery of virally-encoded transgenes into the neonatal mouse brain. In its most basic form, the procedure requires only an ice bucket and a microliter syringe. However, the protocol can also be adapted for use with stereotaxic frames to improve consistency for researchers new to the technique. The method relies on the ability of adeno-associated virus (AAV) to move freely from the cerebral ventricles into the brain parenchyma while the ependymal lining is still immature during the first 12-24 hr after birth. Intraventricular injection of AAV at this age results in widespread transduction of neurons throughout the brain. Expression begins within days of injection and persists for the lifetime of the animal. Viral titer can be adjusted to control the density of transduced neurons, while co-expression of a fluorescent protein provides a vital label of transduced cells. With the rising availability of viral core facilities to provide both off-the-shelf, pre-packaged reagents and custom viral preparation, this approach offers a timely method for manipulating gene expression in the mouse brain that is fast, easy, and far less expensive than traditional germline engineering.

Here we demonstrate a technique for widespread neuronal transduction by intraventricular injection of adeno-associated virus into the neonatal mouse brain. This method provides a rapid and easy way to attain lifelong expression of virally-delivered transgenes.

Kalıcı ve yaygın Nöronal İletim için Yenidoğan Fare Beyin intraserooroventriküler Viral Enjeksiyon

With the pace of scientific advancement accelerating rapidly, new methods are needed for experimental neuroscience to quickly and easily manipulate gene ...

An Ex Vivo Laser-induced Spinal Cord Injury Model to Assess Mechanisms of Axonal Degeneration in Real-time

Injured CNS axons fail to regenerate and often retract away from the injury site. Axons spared from the initial injury may later undergo secondary axonal degeneration. Lack of growth cone formation, regeneration, and loss of additional myelinated axonal projections within the spinal cord greatly limits neurological recovery following injury. To assess how central myelinated axons of the spinal cord respond to injury, we developed an ex vivo living spinal cord model utilizing transgenic mice that express yellow fluorescent protein in axons and a focal and highly reproducible laser-induced spinal cord injury to document the fate of axons and myelin (lipophilic fluorescent dye Nile Red) over time using two-photon excitation time-lapse microscopy. Dynamic processes such as acute axonal injury, axonal retraction, and myelin degeneration are best studied in real-time. However, the non-focal nature of contusion-based injuries and movement artifacts encountered during in vivo spinal cord imaging make differentiating primary and secondary axonal injury responses using high resolution microscopy challenging. The ex vivo spinal cord model described here mimics several aspects of clinically relevant contusion/compression-induced axonal pathologies including axonal swelling, spheroid formation, axonal transection, and peri-axonal swelling providing a useful model to study these dynamic processes in real-time. Major advantages of this model are excellent spatiotemporal resolution that allows differentiation between the primary insult that directly injures axons and secondary injury mechanisms; controlled infusion of reagents directly to the perfusate bathing the cord; precise alterations of the environmental milieu (e.g., calcium, sodium ions, known contributors to axonal injury, but near impossible to manipulate in vivo); and murine models also offer an advantage as they provide an opportunity to visualize and manipulate genetically identified cell populations and subcellular structures. Here, we describe how to isolate and image the living spinal cord from mice to capture dynamics of acute axonal injury.

An Ex Vivo Laser-induced Spinal Cord Injury Model to Assess Mechanisms of Axonal Degeneration in Real-time

We present a protocol utilizing two-photon excitation time-lapse microscopy to simultaneously visualize the dynamics of axon and myelin injuries in real time. This proposed protocol permits studies of both intrinsic and extrinsic factors which can influence central myelinated axon fate after injury and contribute to permanent clinical disability.

Bir<em&gt; Ex vivo</em&gt; Lazer kaynaklı Omurilik Felçlileri Modeli Gerçek zamanlı aksonal Dejenerasyon mekanizmaları değerlendirmek için

Injured CNS axons fail to regenerate and often retract away from the injury site. Axons spared from the initial injury may later undergo secondary axonal ...

A Method to Inflict Closed Head Traumatic Brain Injury in Drosophila

Traumatic brain injury (TBI) affects millions of people each year, causing impairment of physical, cognitive, and behavioral functions and death. Studies using Drosophila have contributed important breakthroughs in understanding neurological processes. Thus, with the goal of understanding the cellular and molecular basis of TBI pathologies in humans, we developed the High Impact Trauma (HIT) device to inflict closed head TBI in flies. Flies subjected to the HIT device display phenotypes consistent with human TBI such as temporary incapacitation and progressive neurodegeneration. The HIT device uses a spring-based mechanism to propel flies against the wall of a vial, causing mechanical damage to the fly brain. The device is inexpensive and easy to construct, its operation is simple and rapid, and it produces reproducible results. Consequently, the HIT device can be combined with existing experimental tools and techniques for flies to address fundamental questions about TBI that can lead to the development of diagnostics and treatments for TBI. In particular, the HIT device can be used to perform large-scale genetic screens to understand the genetic basis of TBI pathologies.

A Method to Inflict Closed Head Traumatic Brain Injury in Drosophila

Here we describe a method to inflict closed head traumatic brain injury (TBI) in Drosophila. This method provides a gateway to investigate the cellular and molecular mechanisms that underlie TBI pathologies using the vast array of experimental tools and techniques available for flies.

Kapalı Başkanı Travmatik Beyin yaralayabilecek Bir Yöntem<em&gt; Drosophila</em

Traumatic brain injury (TBI) affects millions of people each year, causing impairment of physical, cognitive, and behavioral functions and death. Studies ...

Recording EEG in Freely Moving Neonatal Rats Using a Novel Method

EEG is a useful method to detect electrical activity in the brain. Moreover, it is a widely used diagnostic tool for various neurological conditions, such as epilepsy and neurodegenerative disorders. However, it is technically difficult to obtain EEG recordings in neonates as it requires specialized handling and great care. Here, we present a novel method to record EEG in neonatal rat pups (P8-P15). We designed a simple and reliable electrode using computer pin loci; it can be easily implanted into the skull of a rat pup to record high-quality EEG signals in the normal and epileptic brain. Pups were given an intraperitoneal (i.p.) injection of the neurotoxin kainic acid (KA) to induce epileptic seizures. The surgical implantation performed in this procedure is less expensive than other EEG procedures for neonates. This method allows one to record high-quality and stable EEG signals for more than 1 week. Furthermore, this procedure can also be applied to adult rats and mice to study epilepsy or other neurological disorders.

Here, we introduce a novel technique designed to record electroencephalography (EEG) in freely moving neonatal epileptic pups and describe its procedures, features, and applications. This method allows one to record EEG for more than 1 week.

Yeni Bir Yöntemi Kullanarak Serbest Dolaşan Yenidoğan Sıçanlarında EEG Kaydı

EEG is a useful method to detect electrical activity in the brain. Moreover, it is a widely used diagnostic tool for various neurological conditions, such ...

Stereotaxic Surgery for Genetic Manipulation in Striatal Cells of Neonatal Mouse Brains

Many genes are expressed in embryonic brains, and some of them are continuously expressed in the brain after birth. For such persistently expressed genes, they may function to regulate the developmental process and/or physiological function in neonatal brains. To investigate neurobiological functions of specific genes in the brain, it is essential to inactivate genes in the brain. Here, we describe a simple stereotaxic method to inactivate gene expression in the striatum of transgenic mice at neonatal time windows. AAV-eGFP-Cre viruses were microinjected into the striatum of Ai14 reporter gene mice at postnatal day (P) 2 by stereotaxic brain surgery. The tdTomato reporter gene expression was detected in P14 striatum, suggesting a successful Cre-loxP mediated DNA recombination in AAV-transduced striatal cells. We further validated this technique by microinjecting AAV-eGFP-Cre viruses into P2Foxp2fl/fl mice. Double labeling of GFP and Foxp2 showed that GFP-positive cells lacked Foxp2 immunoreactivity in P9 striatum, suggesting the loss of Foxp2 protein in AAV-eGFP-Cre transduced striatal cells. Taken together, these results demonstrate an effective genetic deletion by stereotaxically microinjected AAV-eGFP-Cre viruses in specific neuronal populations in the neonatal brains of floxed transgenic mice. In conclusion, our stereotaxic technique provides an easy and simple platform for genetic manipulation in neonatal mouse brains. The technique can not only be used to delete genes in specific regions of neonatal brains, but it also can be used to inject pharmacological drugs, neuronal tracers, genetically modified optogenetics and chemogenetics proteins, neuronal activity indicators and other reagents into the striatum of neonatal mouse brains.

We describe a protocol of stereotaxic surgery with a homemade head-fixed device for microinjecting reagents into the striatum of neonatal mouse brains. This technique allows genetic manipulation in neuronal cells of specific regions of neonatal mouse brains.

Yenidoğan fare beyin Striatal hücrelerdeki genetik manipülasyon için stereotaksik cerrahi

Many genes are expressed in embryonic brains, and some of them are continuously expressed in the brain after birth. For such persistently expressed genes, ...

A Novel In Vitro Model of Blast Traumatic Brain Injury

Traumatic brain injury is a leading cause of death and disability in military and civilian populations. Blast traumatic brain injury results from the detonation of explosive devices, however, the mechanisms that underlie the brain damage resulting from blast overpressure exposure are not entirely understood and are believed to be unique to this type of brain injury. Preclinical models are crucial tools that contribute to better understand blast-induced brain injury. A novel in vitro blast TBI model was developed using an open-ended shock tube to simulate real-life open-field blast waves modelled by the Friedlander waveform. C57BL/6N mouse organotypic hippocampal slice cultures were exposed to single shock waves and the development of injury was characterized up to 72 h using propidium iodide, a well-established fluorescent marker of cell damage that only penetrates cells with compromised cellular membranes. Propidium iodide fluorescence was significantly higher in the slices exposed to a blast wave when compared with sham slices throughout the duration of the protocol. The brain tissue injury is very reproducible and proportional to the peak overpressure of the shock wave applied.

A Novel In Vitro Model of Blast Traumatic Brain Injury

This paper describes a novel model of primary blast traumatic brain injury. A compressed-air driven shock tube is used to expose in vitro mouse hippocampal slice cultures to a single shock wave. This is a simple and rapid protocol generating a reproducible brain tissue injury with a high throughput.

Patlama travmatik beyin hasarı roman Vitro modeli

Traumatic brain injury is a leading cause of death and disability in military and civilian populations. Blast traumatic brain injury results from the ...

Effects of Blast-induced Neurotrauma on Pressurized Rodent Middle Cerebral Arteries

Though there have been studies on the histopathological and behavioral effects of blast exposure, fewer have been dedicated to blast&#39;s cerebral vascular effects. Impact (i.e., non-blast) traumatic brain injury (TBI) is known to decrease pressure autoregulation in the cerebral vasculature in both humans and experimental animals. The hypothesis that blast-induced traumatic brain injury (bTBI), like impact TBI, results in impaired cerebral vascular reactivity was tested by measuring myogenic dilatory responses to reduced intravascular pressure in rodent middle cerebral arterial (MCA) segments from rats subjected to mild bTBI using an Advanced Blast Simulator (ABS) shock tube. Adult, male Sprague-Dawley rats were anesthetized, intubated, ventilated and prepared for Sham bTBI (identical manipulation and anesthesia except for blast injury) or mild bTBI. Rats were randomly assigned to receive Sham bTBI or mild bTBI followed by sacrifice 30 or 60 min post-injury. Immediately after bTBI, righting reflex (RR) suppression times were assessed, euthanasia at the time points post-injury was completed, the brain was harvested and the individual MCA segments were collected, mounted and pressurized. As the intraluminal pressure perfused through the arterial segments was reduced in 20 mmHg increments from 100 to 20 mmHg, MCA diameters were measured and recorded. With decreasing intraluminal pressure, MCA diameters steadily increased significantly above baseline in the Sham bTBI groups while MCA dilator responses were significantly reduced (p &#60; 0.05) in both bTBI groups as evidenced by the impaired, smaller MCA diameters recorded for the bTBI groups. In addition, RR suppression in the bTBI groups was significantly (p &#60; 0.05) higher than in the Sham bTBI groups. MCA&#39;s collected from the Sham bTBI groups exhibited typical vasodilatory properties to decreases in intraluminal pressure while MCA&#39;s collected following bTBI exhibited significantly impaired myogenic vasodilatory responses to reduced pressure that persisted for at least 60 min after bTBI.

Here, we present a protocol to describe methods for ex vivo vascular reactivity determination following a primary blast traumatic brain injury (bTBI) using isolated, pressurized, rodent middle cerebral arterial (MCA) segments. bTBI induction is accomplished using a shock tube, also known as an Advanced Blast Simulator (ABS) device.

Serebral arterler patlama kaynaklı Neurotrauma etkilerini basınçlı kemirgen orta

Though there have been studies on the histopathological and behavioral effects of blast exposure, fewer have been dedicated to blast&#39;s cerebral ...

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury

There is an ongoing need for clinically relevant models of perinatal infection and hypoxia-ischemia (HI) in which to test therapeutic interventions for infants with the neurological sequela of prematurity. Ferrets are ideal candidates for modeling the preterm human brain, as they are born lissencephalic and develop gyrencephalic brains postnatally. At birth, ferret brain development is similar to a 13 week human fetus, with postnatal-day (P) 17 kits considered to be equivalent to an infant at 32&#8211;36 weeks&#39; gestation. We describe an injury model in the P17 ferret, where lipopolysaccharide administration is followed by bilateral cerebral ischemia, hypoxia, and hyperoxia. This simulates the complex interaction of prolonged inflammation, ischemia, hypoxia, and oxidative stress experienced in a number of neonates who develop brain injury. Injured animals display a range of gross injury severity, with morphological changes in the brain including narrowing of multiple cortical gyri and associated sulci. Injured animals also show slowed reflex development, slower and more variable speed of locomotion in an automated catwalk, and decreased exploration in an open field. This model provides a platform in which to test putative therapies for infants with neonatal encephalopathy associated with inflammation and HI, study mechanisms of injury that affect cortical development, and investigate pathways that provide resilience in unaffected animals.

The method describes inflammation-sensitized hypoxic-ischemic and hyperoxic brain injury in the P17 ferret to model the complex interaction between prolonged inflammation and oxidative brain injury experienced in a number of late preterm infants.

İnflamasyon duyarlıgeç Preterm Hipoksik-iskemik Beyin Hasarı Bir Gelincik Modeli

There is an ongoing need for clinically relevant models of perinatal infection and hypoxia-ischemia (HI) in which to test therapeutic interventions for ...

Intra-Arterial Delivery of Neural Stem Cells to the Rat and Mouse Brain: Application to Cerebral Ischemia

Neural stem cell (NSC) therapy is an emerging innovative treatment for stroke, traumatic brain injury and neurodegenerative disorders. As compared to intracranial delivery, intra-arterial administration of NSCs is less invasive and produces a more diffuse distribution of NSCs within the brain parenchyma. Further, intra-arterial delivery allows the first-pass effect in the brain circulation, lessening the potential for trapping of cells in peripheral organs, such as liver and spleen, a complication associated with peripheral injections. Here, we detail the methodology, in both mice and rats, for delivery of NSCs through the common carotid artery (mouse) or external carotid artery (rat) to the ipsilateral hemisphere after an ischemic stroke. Using GFP-labeled NSCs, we illustrate the widespread distribution achieved throughout the rodent ipsilateral hemisphere at 1 d, 1 week and 4 weeks after postischemic delivery, with a higher density in or near the ischemic injury site. In addition to long-term survival, we show evidence of differentiation of GFP-labeled cells at 4 weeks. The intra-arterial delivery approach described here for NSCs can also be used for administration of therapeutic compounds, and thus has broad applicability to varied CNS injury and disease models across multiple species.

A method for delivering neural stem cells, adaptable for injecting solutions or suspensions, through the common carotid artery (mouse) or external carotid artery (rat) after ischemic stroke is reported. Injected cells are distributed broadly throughout the brain parenchyma and can be detected up to 30 d after delivery.

Nöral Kök Hücrelerin Sıçan ve Fare Beynine İntra-Arteriyel Teslimatı: Serebral İskemiye Uygulama

Neural stem cell (NSC) therapy is an emerging innovative treatment for stroke, traumatic brain injury and neurodegenerative disorders. As compared to ...