この研究は、国立研究財団 (NRF 2014R1A2A1A11052042; 2015M3A9B4067068)、科学省と技術、韓国、韓国健康技術 R & D プロジェクト (HI16C1012)、厚生労働省からの助成金によって支えられた &福祉・韓国・延世大学医学 (6-2016-0126) の「東和」学部研究支援プログラム。

すべての動物施設評価認定の研究所動物ケア (AAALAC) 協会の認定を受けて、食べ物を与えられる (27 × 22.5 × 14 cm3) 標準的な檻の中で収容され、水を交互に 12 h/暗下で自由サイクル。著者動物保護の規則に従い、実験手順が承認された機関動物ケアおよび使用委員会の延世大学医科大学 (IACUC 号 2010-0252; 2013-0220)。
1. こんにちは新生児の脳損傷マウスモデル
<ol><li>イソフルランと子犬を麻酔します。<ol>
<li>子犬 (5 未満) を麻酔ボックスに置き、ふたを閉じる。</li>
		<li>約 15 分間; 麻酔を入れますガスとイソフルラン テーブル トップ麻酔機を使用して調整します。1.5 L/分調整麻酔導入の 3-5% にイソフルラン気化器に酸素流量を調整します。</li>
		<li>15 分後に麻酔の維持のための 1-2% にイソフルラン気化器を調整します。</li>
	</ol>
</li>
	<li>解剖顕微鏡 (研究者に直面して腹部) の下で完全に麻酔をかけられた子犬を置き、テープで固定します。</li>
	<li>滅菌はさみを使って首で ~0.7-mm 切開を行います。</li>
	<li>慎重に滅菌鉗子を使用して脂肪組織を除去し、一方的な右頸動脈を公開します。</li>
	<li>5-0 吸収性縫合糸で一方的な右頚動脈を結紮します。</li>
	<li>5-0 縫合糸で首の切開部を縫合します。</li>
	<li>回復の 1 h に 37 ° C の暖かい低酸素室の中には、それぞれの子犬を配置します。商工会議所のふたは閉じないでください。</li>
	<li>手術後 1 h 子犬が完全に目を覚まし、低酸素室蓋を閉じるし、(8% O2と 92% N2) 低酸素の条件を確立するガスのレベルを減少させます。</li>
	<li>低酸素の 90 分後、子犬をケージに戻ります。</li>
	<li>こんにちは脳損傷後 1 週間は、手順 1 を繰り返します。<ol>
<li>麻酔後滅菌ハサミ鉗子右半球の後外側領域に脳の病変を識別すると、頭皮の切開を行います。 注: この治療は仔ラットの低酸素症を誘発します。存在とすべてのマウスにおける脳損傷の程度は、半透明頭蓋骨を通して肉眼で視覚的に評価されます。サイズまたは変色 (すなわち、脳障害) のボリュームにより、子犬はグループに分類されます。表示される大脳皮質損傷がない場合マウスは「大脳皮質損傷なし」グループに分類されます。可視皮質障害 (すなわち、右半球の病変) がある場合、マウスは「大脳皮質損傷」グループに分類されます。脳サンプルの形態が犠牲1,2,3の時に明確に定義されている場合、グループを変更できるマウスのグループへの分類は、術後後 1 週間を行われる、ので 4。</li>
	</ol>
</li>
</ol><img alt="Figure 1" class="xfigimg" src="/files/ftp_upload/55838/55838fig1v3.jpg"> 図 1: マウスの新生児のこんにちは脳損傷のモデル化。 (A) 7 日齢マウスの子犬が手術し、片側右頚動脈を結紮します。(B) 子犬は 8% O2と 92% N2で 90 分に低酸素室の中に置かれました。(C、D、および E)新生児こんにちは外傷による脳損傷の様々 な重症度を示したし、損傷の程度に基づいて分類されました。14 日に脳を入手し、病変が, 可視化されました。(C)、「ない皮質損傷」に分類される脳のイメージ。両方 (D) および (E)「大脳皮質損傷」グループに分類されました。(F、G、および H)(C) の代表的な MRI (D) および (E) マウス、それぞれ。(F) 海馬での被害は、黄色の矢印で示され、右半球の病変も (G および H) の黄色の矢印で示されます。スケール バー 1 mm =<a href="http://cloudflare.jove.com/files/ftp_upload/55838/55838fig1v3large.jpg" target="_blank">この図の拡大版を表示するのにはここをクリックしてください</a>。
2. 新生児の行動テスト
注: ここでは、行動のテストは、6 週齢で行われました。
<ol><li>
受動的回避反応タスク。 注: 学習と嫌悪刺激の回避に基づくメモリ関数を評価するには、パット ステップ 2 コンパートメントは実施13,14,15,16をする必要があります。<ol>
<li>パット装置のプレキシ ガラス シャトル ボックス (41.5 × 21 × 35 cm3) の明るい区画にマウスを配置します。</li>
		<li>後 30 秒、ギロチン ドアを開き、暗い区画に移動するマウスの遅延時間を記録 (最大 300 s)。</li>
		<li>マウスのすべての 4 つの手足が完全に暗い室内は、ギロチンのドアを閉じます。</li>
		<li>電気フット ショックを管理 (0.5 mA) 2 s と檻に戻るマウス。</li>
		<li>電気フット ショック後明るい区画 24 h でマウスを交換してください。</li>
		<li>完全に明るい区画に配置した後マウス ギロチン ドア 10 s を開き、暗い区画に移動するマウスの遅延時間を記録 (最大 300 s)。</li>
	</ol>
</li>
	<li>
歩行テストをはしご。 注: はしごラング歩行タスクで質的な組み合わせることにより運動機能の微妙な障害および熟練した歩行17,18の定量分析とを区別できます。<ol>
<li>ビデオ カメラをオンにします。</li>
		<li>はしごのスタート パネルにマウスを置き、すぐに録音を開始します。</li>
		<li>マウスの肢に焦点を当て、映像を記録します。</li>
		<li>マウスに触れるはしごの最後のパネルの記録を停止します。行ったり来たりの旅を 4 回繰り返します。</li>
		<li>ビデオの記録を分析し、手動で次のように各前肢の伝票の数をカウントします。<ol>
<li>低速のコンピューター上のビデオの録画 (0.1 x) と手動での手順をカウントします。</li>
		</ol>
</li>
	</ol>
</li>
	<li>
グリップ強度テスト。 メモ: グリップ強度テストはプッシュプル ゲージを含むグリップ強度メーターを使用して実行されます。<ol>
<li>アクリル パネルにグリップ力装置を修正します。</li>
		<li>アクリル パネルにマウスを置き、しっぽを保持します。<ol>
<li>マウスがアクセスできるように、尾を持っている手とグリップ装置の金属の線を移動します。</li>
		</ol>
</li>
		<li>マウス グリップ金属ワイヤ (直径 2 mm); 三角形部分まで、複数の試験を許可します。ピーク力はグラムに装置によって自動的に登録されます。 注: 分析19,20,21の 3 つの試験の平均ピーク力を使用します。</li>
	</ol>
</li>
</ol>

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著者は競合する興味を持ってないです。

本研究では、HI P7 10 CD-1 マウスの新生児脳障害し、関連する認知およびモーター欠損で脳障害を識別しました。この中に、片側の右頚動脈の閉塞は重要でした。この手順で動脈を破損し、破れたでした。動脈涙を経験したほとんどの子犬が死亡しました。逆に、研究者は、一方的な右頚動脈ではなく別の血液静脈を結紮、子犬の脳は少しだけ破損しているし、重要な表現が認められなかった<s...

幼い頃 (約 1,000 人の子供あたりの 2 人の患者)1,2,3,4,5中に新生児のこんにちは脳損傷が発生します。新生児こんにちは脳損傷に関する研究が重要であり、確立された新生児こんにちは脳損傷マウス モデルを用いた体内こんにちは脳損傷の臨床研究を促進できます。
ラット6従来の HI モデルが使用されます。新生児モデルの米ヴァンヌッチ メソッドは P7 ラット7,8よく使用されます。ただし、ラットおよびマウスなのでわずかに異なる9,10、にもかかわらず両方の齧歯動物を行った修正米ヴァンヌッチ法 P7-10 P7 10 ある期間であることを示した前の研究を基に CD 1 子犬の特徴未熟なオリゴデンドロ サイト、人間用語 P011,12に対応します。新生児のこんにちのマウスモデルは P7 10 子犬の両方一側内頚動脈の結紮とマウスの 8% の酸素と低酸素への露出によって確立されます。
マウス右半球の後外側領域にさまざまな脳の病変の程度を示したプロシージャに服従します。認知およびモーター欠損、PAT に基づく神経行動学的評価を識別し、はしごの歩行テスト、およびグリップ強度テストを行った。非運営 (すなわち、通常) とこんにちはマウスとの違いを分析しました。この作品は、HI マウス モデルに関する基本的な情報を示します。MRI 画像は、運動と認知機能テストを使用して脳の損傷の重症度に応じて、分離、異なった表現型を示しています。

<table><tbody><tr><td>Hypoxic chamber</td><td>Jeung Do Bio &amp;amp; Plant Co</td><td>Experimental Builder</td><td></td></tr><tr><td>PAT apparatus</td><td>Jeung Do Bio &amp;amp; Plant Co</td><td>Experimental Builder</td><td></td></tr><tr><td>The ladder rung walking</td><td>Jeung Do Bio &amp;amp; Plant Co</td><td>Experimental Builder</td><td></td></tr><tr><td>SDI Grip Strength System</td><td>San Diego Instruments Inc.</td><td></td><td></td></tr><tr><td>Grip-Strength Meter</td><td>Ugo Basile</td><td>47200</td><td></td></tr><tr><td>Harvard Apparatus Fluovac anesthetizing system&amp;nbsp;</td><td>Harvard Apparatus</td><td></td><td></td></tr><tr><td>Anesthetizing box</td><td></td><td></td><td>acryl box</td></tr><tr><td>I-Fran Liquid (Isofluorane)</td><td>Hana Pharm. Co., Ltd.</td><td></td><td>General Anesthetics ( isoflurane 100ml)</td></tr><tr><td>CD-1 mice</td><td>Orient Co., Ltd.</td><td></td><td></td></tr><tr><td>Blue Nylon Mono Non-Absorbbable suture 5-0 50cm</td><td>Ailee Co., Ltd.</td><td>NB 521</td><td></td></tr><tr><td>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

CD-1 マウス新生児低酸素性虚血性 (HI) モデルを作成するに一側内頚動脈閉塞を実施し、に比べて非操作 (つまり、これらのマウスの神経行動学的機能を研究することによって新生児こんにちは脳損傷の効果を調査通常の) マウス。調査中, 米ヴァンヌッチ メソッドは生後 7-10 (P7-10) マウスの新生児のこんにちは脳の損傷を誘導するために使用されました。こんにちは操作は、一方的な頚動脈結紮と低酸素症 (8% O2と 90 分の 92% N2 ) への露出によって、子犬に実行されました。術後、1 週間破損した脳半透明頭蓋骨を通して肉眼で評価され、不在 (「大脳皮質損傷なし」グループ) や大脳皮質損傷の存在 (「大脳皮質損傷」グループ) に基づくサブグループに分類されました。など右半球の病変。週 6、認知・運動機能を評価する以下の神経行動学的検査を行った: 受動的回避反応タスク (PAT)、はしご歩行テスト、およびグリップ強度テスト。これらの行動テスト新生児こんにちは脳損傷の影響を決定する上で有用ですが、その他の神経変性疾患のマウス ・ モデルで使用されます。本研究では、新生児こんにちは脳損傷マウスは右半球損傷に対応したモーターの赤字を示した。行動テスト結果、脳性麻痺または新生児脳梗塞など、人間の新生児こんにちは患者にみられる欠損に関連します。この研究では、新生児のこんにちは脳損傷のマウス モデルは運動障害と非操作マウスに比べて認知障害の程度が異なるを示したおよび設立されました。この作品は、こんにちマウス モデルの基本情報を説明します。MRI 画像は、運動と認知機能テストで脳の損傷の重症度に応じて区切られた異なる表現型を示しています。

すべてのデータは、平均値 (SEM) の平均 ± 標準誤差として表されます。独立した、またはtを使用して 2 つのグループ間の変数の比較を行った-SPSS の統計ソフトウェアのテストします。P-値 < 0.05 は、統計的に有意と考えられていた。
新生児こんにちは外傷による脳損傷の別の重要度を示したし、それに応じて?...

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

生後に一側内頚動脈閉塞を行った 7 10 CD-1 マウス新生児低酸素性虚血性 (HI) モデルを作成する子犬とこんにちは脳損傷の効果を検討しました。非運営正常なマウスと比較してこれらのマウスの神経行動学的機能を検討した.

新生児低酸素性虚血性脳損傷のマウス モデルにおける神経行動学的評価

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 ビュー.  Yonsei University College of Medicine. 生後に一側内頚動脈閉塞を行った 7 10 CD-1 マウス新生児低酸素性虚血性 (HI) モデルを作成する子犬とこんにちは脳損傷の効果を検討しました。非運営正常なマウスと比較してこれらのマウスの神経行動学的機能を検討した.

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

Mouse Models of Periventricular Leukomalacia

We describe a protocol for establishing mouse models of periventricular leukomalacia (PVL). PVL is the predominant form of brain injury in premature infants and the most common antecedent of cerebral palsy. PVL is characterized by periventricular white matter damage with prominent oligodendroglial injury. Hypoxia/ischemia with or without systemic infection/inflammation are the primary causes of PVL. We use P6 mice to create models of neonatal brain injury by the induction of hypoxia/ischemia with or without systemic infection/inflammation with unilateral carotid ligation followed by exposure to hypoxia with or without injection of the endotoxin lipopolysaccharide (LPS). Immunohistochemistry of myelin basic protein (MBP) or O1 and electron microscopic examination show prominent myelin loss in cerebral white matter with additional damage to the hippocampus and thalamus. Establishment of mouse models of PVL will greatly facilitate the study of disease pathogenesis using available transgenic mouse strains, conduction of drug trials in a relatively high throughput manner to identify candidate therapeutic agents, and testing of stem cell transplantation using immunodeficiency mouse strains.

We established mouse models of periventricular leukomalacia (PVL), the predominant brain injury in premature infants characterized by periventricular white matter lesions. Hypoxia/ischemia with/without systemic infection are the primary causes of PVL. Unilateral carotid ligation and hypoxia exposure with/without lipopolysaccharide injection creates PVL-like lesions in P6 mice.

脳室周囲白質軟化症のマウスモデル

We describe a protocol for establishing mouse models of periventricular leukomalacia (PVL). PVL is the predominant form of brain injury in premature ...

神経科学

Neurodevelopmental Reflex Testing in Neonatal Rat Pups

Neurodevelopmental reflex testing is commonly used in clinical practice to assess the maturation of the nervous system. Neurodevelopmental reflexes are also referred to as primitive reflexes. They are sensitive and consistent with later outcomes. Abnormal reflexes are described as an absence, persistence, reappearance, or latency of reflexes, which are predictive indices of infants that are at high risk for neurodevelopmental disorders. Animal models of neurodevelopmental disabilities, such as cerebral palsy, often display aberrant developmental reflexes, as would be observed in human infants. The techniques described assess a variety of neurodevelopmental reflexes in neonatal rats. Neurodevelopmental reflex testing offers the investigator a testing method that is not otherwise available in such young animals. The methodology presented here aims to assist investigators in examining developmental milestones in neonatal rats as a method of detecting early-onset brain injury and/or determining the effectiveness of therapeutic interventions. The methodology presented here aims to provide a general guideline for investigators.

Behavioral testing is the gold standard for determining outcomes following brain injury, and can identify the presence of developmental disabilities in infants and children. Neurodevelopmental reflexes are an early indicator of these abnormalities. A host of easily accomplished developmental reflex tests in the neonatal rodent were developed and described here.

新生ラット仔における神経発達レフレックステスト

Neurodevelopmental reflex testing is commonly used in clinical practice to assess the maturation of the nervous system. Neurodevelopmental reflexes are ...

行動学

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia

Hypoxic-Ischemic Encephalopathy (HIE) is the consequence of systemic asphyxia occurring at birth. Twenty five percent of neonates with HIE develop severe and permanent neuropsychological sequelae, including mental retardation, cerebral palsy, and epilepsy. The outcomes of HIE are devastating and permanent, making it critical to identify and develop therapeutic strategies to reduce brain injury in newborns with HIE. To that end, the neonatal rat model for hypoxic-ischemic brain injury has been developed to model this human condition. The HIE model was first validated by Vannucci et al 1 and has since been extensively used to identify mechanisms of brain injury resulting from perinatal hypoxia-ischemia 2 and to test potential therapeutic interventions 3,4. The HIE model is a two step process and involves the ligation of the left common carotid artery followed by exposure to a hypoxic environment. Cerebral blood flow (CBF) in the hemisphere ipsilateral to the ligated carotid artery does not decrease because of the collateral blood flow via the circle of Willis; however with lower oxygen tension, the CBF in the ipsilateral hemisphere decreases significantly and results in unilateral ischemic injury. The use of 2,3,5-triphenyltetrazolium chloride (TTC) to stain and identify ischemic brain tissue was originally developed for adult models of rodent cerebral ischemia 5, and is used to evaluate the extent of cerebral infarctin at early time points up to 72 hours after the ischemic event 6. In this video, we demonstrate the hypoxic-ischemic injury model in postnatal rat brain and the evaluation of the infarct size using TTC staining.

The postnatal rat model for hypoxic-ischemic brain injury is a well-established model of human neonatal hypoxic ischemic encephalopathy (HIE). In this article, we describe the model of HIE in post-natal rat pups.

周産期虚血低酸素虚血性脳症モデル

Hypoxic-Ischemic Encephalopathy (HIE) is the consequence of systemic asphyxia occurring at birth. Twenty five percent of neonates with HIE develop severe ...

生物学

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy

Birth asphyxia, which causes hypoxic-ischemic encephalopathy (HIE), accounts for 0.66 million deaths worldwide each year, about a quarter of the world&#8217;s 2.9 million neonatal deaths. Animal models of HIE have contributed to the understanding of the pathophysiology in HIE, and have highlighted the dynamic process that occur in brain injury due to perinatal asphyxia. Thus, animal studies have suggested a time-window for post-insult treatment strategies. Hypothermia has been tested as a treatment for HIE in pdiglet models and subsequently proven effective in clinical trials. Variations of the model have been applied in the study of adjunctive neuroprotective methods and piglet studies of xenon and melatonin have led to clinical phase I and II trials1,2. The piglet HIE model is further used for neonatal resuscitation- and hemodynamic studies as well as in investigations of cerebral hypoxia on a cellular level. However, it is a technically challenging model and variations in the protocol may result in either too mild or too severe brain injury. In this article, we demonstrate the technical procedures necessary for establishing a stable piglet model of neonatal HIE. First, the newborn piglet (&#60; 24 hr old, median weight 1500 g) is anesthetized, intubated, and monitored in a setup comparable to that found in a neonatal intensive care unit. Global hypoxia-ischemia is induced by lowering the inspiratory oxygen fraction to achieve global hypoxia, ischemia through hypotension and a flat trace amplitude integrated EEG (aEEG) indicative of cerebral hypoxia. Survival is promoted by adjusting oxygenation according to the aEEG response and blood pressure. Brain injury is quantified by histopathology and magnetic resonance imaging after 72 hr.

Hypoxic-ischemic encephalopathy following perinatal asphyxia can be studied using animal models. We demonstrate the procedures necessary for establishing a piglet model of neonatal hypoxic-ischemic encephalopathy.

新生児低酸素性虚血性脳症の子豚モデル

Birth asphyxia, which causes hypoxic-ischemic encephalopathy (HIE), accounts for 0.66 million deaths worldwide each year, about a quarter of the ...

医学

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders

Induction of phosphorylated extracellular-regulated kinase (pERK) is a reliable molecular readout of learning-dependent neuronal activation. Here, we describe a pERK immunohistochemistry protocol to study the profile of hippocampal neuron activation following exposure to a spatial learning task in a mouse model characterized by cognitive deficits of neurodevelopmental origin. Specifically, we used pERK immunostaining to study neuronal activation following Morris water maze (MWM, a classical hippocampal-dependent learning task) in Engrailed-2 knockout (En2-/-) mice, a model of autism spectrum disorders (ASD). As compared to wild-type (WT) controls, En2-/- mice showed significant spatial learning deficits in the MWM. After MWM, significant differences in the number of pERK-positive neurons were detected in specific hippocampal subfields of En2-/- mice, as compared to WT animals. Thus, our protocol can robustly detect differences in pERK-positive neurons associated to hippocampal-dependent learning impairment in a mouse model of ASD. More generally, our protocol can be applied to investigate the profile of hippocampal neuron activation in both genetic or pharmacological mouse models characterized by cognitive deficits.

We describe an immunohistochemistry protocol to study the profile of hippocampal neuron activation following exposure to a spatial learning task in a mouse model characterized by cognitive deficits of neurodevelopmental origin. This protocol can be applied to both genetic or pharmacological mouse models characterized by cognitive deficits.

神経発達障害のマウスモデルにおける空間学習した後、海馬ニューロン活動の免疫組織化学的可視化

Induction of phosphorylated extracellular-regulated kinase (pERK) is a reliable molecular readout of learning-dependent neuronal activation. Here, we ...

A Battery of Motor Tests in a Neonatal Mouse Model of Cerebral Palsy

As the sheer number of transgenic mice strains grow and rodent models of pediatric disease increase, there is an expanding need for a comprehensive, standardized battery of neonatal mouse motor tests. These tests can validate injury or disease models, determine treatment efficacy and/or assess motor behaviors in new transgenic strains. This paper presents a series of neonatal motor tests to evaluate general motor function, including ambulation, hindlimb foot angle, surface righting, negative geotaxis, front- and hindlimb suspension, grasping reflex, four limb grip strength and cliff aversion. Mice between the ages of post-natal day 2 to 14 can be used. In addition, these tests can be used for a wide range of neurological and neuromuscular pathologies, including cerebral palsy, hypoxic-ischemic encephalopathy, traumatic brain injury, spinal cord injury, neurodegenerative diseases, and neuromuscular disorders. These tests can also be used to determine the effects of pharmacological agents, as well as other types of therapeutic interventions. In this paper, motor deficits were evaluated in a novel neonatal mouse model of cerebral palsy that combines hypoxia, ischemia and inflammation. Forty-eight hours after injury, five tests out of the nine showed significant motor deficits: ambulation, hindlimb angle, hindlimb suspension, four limb grip strength, and grasping reflex. These tests revealed weakness in the hindlimbs, as well as fine motor skills such as grasping, which are similar to the motor deficits seen in human cerebral palsy patients.

Presented is a concise battery of mouse neonatal motor tests. Using these tests, neonatal motor deficits can be demonstrated in a variety of neonatal motor disorders. By having a standardized set of tests, results from different studies can be compared, allowing for better and accurate reporting between groups.

脳性麻痺の新生児マウスモデルにおける運動テストのバッテリー

As the sheer number of transgenic mice strains grow and rodent models of pediatric disease increase, there is an expanding need for a comprehensive, ...

A Controlled Mouse Model for Neonatal Polymicrobial Sepsis

Neonatal sepsis remains a global burden. A preclinical model to screen effective prophylactic or therapeutic interventions is needed. Neonatal mouse polymicrobial sepsis can be induced by injecting cecal slurry intraperitoneally into day of life 7 mice and monitoring them for the following week. Presented here are the detailed steps necessary for the implementation of this neonatal sepsis model. This includes making a homogeneous cecal slurry stock, diluting it to a weight- and litter-adjusted dose, an outline of the monitoring schedule, and a definition of observed health categories used to define humane endpoints. The generation of a homogeneous cecal slurry stock from pooled donors allows for the administration into many litters over time, reducing the variation between donors, and preventing the use of potentially toxic glycerol. The monitoring strategy used allows for the anticipation of survival outcome and the identification of mice that would later progress to death, allowing for an earlier identification of the humane endpoint. Two main behavioral features are used to define the health scores, namely, the ability of the neonatal mice to right themselves when placed on their back and their level of mobility. These criteria could potentially be applied to address humane endpoints in other studies of neonatal disease in mice, as long as a pilot study is performed to confirm accuracy. In conclusion, this approach provides a standardized method to model newborn sepsis in mice, while providing resources to assess animal welfare used to define early humane endpoints for challenged animals.

This protocol provides the necessary steps to establish and evaluate neonatal sepsis in 7-day-old mice.

新生児モデル敗血症マウスの制御モデル

Neonatal sepsis remains a global burden. A preclinical model to screen effective prophylactic or therapeutic interventions is needed. Neonatal mouse ...

免疫・感染学

Continuous Video Electroencephalogram during Hypoxia-Ischemia in Neonatal Mice

Hypoxia ischemia is the most common cause of neonatal seizures. Animal models are crucial for understanding the mechanisms and physiology underlying neonatal seizures and hypoxia ischemia. This manuscript describes a method for continuous video electroencephalogram (EEG) monitoring in neonatal mice to detect seizures and analyze EEG background during hypoxia ischemia. Use of video and EEG in conjunction allows description of seizure semiology and confirmation of seizures. This method also allows analysis of power spectrograms and EEG background pattern trends over the experimental time period. In this hypoxia ischemia model, the method allows EEG recording prior to injury to obtain a normative baseline and during injury and recovery. Total monitoring time is limited by the inability to separate pups from the mother for longer than four hours. Although, we have used a model of hypoxic-ischemic seizures in this manuscript, this method for neonatal video EEG monitoring could be applied to diverse disease and seizure models in rodents.

This manuscript describes a method for continuous video EEG recordings using multiple depth electrodes in neonatal mice undergoing hypoxia-ischemia.

新生児マウスにおける低酸素虚血期における連続映像脳波

Hypoxia ischemia is the most common cause of neonatal seizures. Animal models are crucial for understanding the mechanisms and physiology underlying ...

Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy

Perinatal hypoxic-ischemic encephalopathy (HIE) is an acute disease that may afflict newborns, resulting in variable long- and short-term neurodevelopmental outcomes. Early diagnosis is critical to identifying infants who may benefit from intervention; however, early diagnosis relies heavily on clinical criteria. No molecular or radiological tests have shown promise in detecting early cerebral injury. Studies have shown that magnetic resonance imaging (MRI) can show changes in both blood flow/ischemia and metabolic disruption. However, they have all been used to evaluate the secondary phase of the disease (&gt;12 h) after the onset of the injury. Early diagnosis is critical to rapidly starting therapeutic hypothermia in eligible infants, which is currently recommended to be initiated within 6 h of birth. The rat model of hypoxic-ischemic injury was developed in 1981 and has been validated and used extensively to study changes in brain perfusion, cerebral injury markers, and morphology. However, it has primarily been used as a "late model", evaluating injury several days after the initial ischemic insult. The model has been known to have poor sensitivity in evaluating reliable and reproducible early cerebral changes. The objective of this study was to develop a reliable model to study early gross morphological and radiological markers of HIE using pathological staining and cerebral magnetic resonance imaging/magnetic resonance spectroscopy.

<meta charset="utf8"></head><body>新生児低酸素性虚血性脳症のラットモデルを用いた脳損傷の早期病理学的および磁気共鳴検出

The present protocol describes a rodent model of newborn hypoxic-ischemic injury for identifying early changes in cerebral tissue by gross morphology and magnetic resonance imaging. This has benefits over existing models, which can be used to study late injury but do not allow the evaluation of reproducible early changes.

新生児低酸素性虚血性脳損傷のマウスモデルにおける神経行動学的評価

要約

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この動画の章

脳室周囲白質軟化症のマウスモデル

新生ラット仔における神経発達レフレックステスト

周産期虚血低酸素虚血性脳症モデル

新生児低酸素性虚血性脳症の子豚モデル

神経発達障害のマウスモデルにおける空間学習した後、海馬ニューロン活動の免疫組織化学的可視化

脳性麻痺の新生児マウスモデルにおける運動テストのバッテリー

新生児モデル敗血症マウスの制御モデル

新生児マウスにおける低酸素虚血期における連続映像脳波

新生児低酸素性虚血性脳症のラットモデルを用いた脳損傷の早期病理学的および磁気共鳴検出

新生児低酸素性虚血性脳症のラットモデルを用いた脳損傷の早期病理学的および磁気共鳴検出

新生児低酸素性虚血性脳損傷のマウス モデルにおける神経行動学的評価

要約

さらに動画を探す

この動画の章

脳室周囲白質軟化症のマウスモデル

新生ラット仔における神経発達レフレックステスト

周産期虚血低酸素虚血性脳症モデル

新生児低酸素性虚血性脳症の子豚モデル

神経発達障害のマウスモデルにおける空間学習した後、海馬ニューロン活動の免疫組織化学的可視化

脳性麻痺の新生児マウスモデルにおける運動テストのバッテリー

新生児モデル敗血症マウスの制御モデル

新生児マウスにおける低酸素虚血期における連続映像脳波

新生児低酸素性虚血性脳症のラットモデルを用いた脳損傷の早期病理学的および磁気共鳴検出

新生児低酸素性虚血性脳症のラットモデルを用いた脳損傷の早期病理学的および磁気共鳴検出

新生児低酸素性虚血性脳損傷のマウスモデルにおける神経行動学的評価