Infarct volume quantification in mouse focal cerebral ischemia: a comparison of triphenyltetrazolium chloride and cresyl violet staining techniques

Türeyen, Kudret; Vemuganti, Raghu; Sailor, Kurt A.; Dempsey, Robert J.

doi:10.1016/j.jneumeth.2004.04.029

Cited by 151 publications

(109 citation statements)

References 19 publications

(35 reference statements)

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“…The 2,3,5-triphenyltetrazolium chloride method rests on the functioning of mitochondrial enzymes (Liszczak et al, 1984) and has been used by several groups to mark cerebral infarct area (Bose et al, 1988;Park et al, 1988;Hatfield et al, 1991;Goldlust et al, 1996;Kuroiwa et al, 2009;Popp et al, 2009). An obvious advantage of this method is its easy applicability, suitability for infarct volume evaluation and the immediate availability of results (Bederson et al, 1986;Mathews et al, 2000;Türeyen et al, 2004;Popp et al, 2009). Evidence shows that only a sustained ischemia can result in an early (i.e., 4 h after ischemia onset) reliable TTC stain (Popp et al, 2009), agreement with the fact that irreversible injury to mitochondria in brain cells may not occur until after a long period of ischemia (Rehncrona et al, 1979).…”

Section: Ttc Stainingmentioning

confidence: 79%

Changes in Hippocampal Neuronal Activity During and After Unilateral Selective Hippocampal IschemiaIn Vivo

Barth¹,

Módy²

2011

J. Neurosci.

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The hippocampal formation is one of the brain regions most sensitive to ischemic damage. However, there are no studies about changes in hippocampal neuronal activity during and after a selective unilateral hippocampal ischemia. We developed a novel unilateral cerebrovascular ischemia model in mice that selectively shuts down blood supply to the ipsilateral hippocampal formation. Using a modified version of the photothrombotic method, we stereotaxically targeted the initial ascending part of the longitudinal hippocampal artery in urethane anesthetized and rose bengal-injected mice. To block blood flow in the targeted artery, we photoactivated the rose bengal by illuminating the longitudinal hippocampal artery through an optical fiber inserted into the brain. In vivo field potential recordings in the CA1 region of the hippocampus before, during and after the induction of ischemia demonstrated a high-frequency discharge (HFD) reaching frequencies of Ͼ300 Hz and lasting 7-24 s during the illumination consistent with a massive synchronous neuronal activity. The HFD was invariably followed by a DC voltage shift and a decreased activity at both low (30 -57 Hz)-and high (63-119 Hz)-gamma frequencies. This decrease in gamma activity lasted for the entire duration of the recordings (ϳ160 min) following ischemia. The contralateral hippocampus displayed HFDs but with different frequency spectra and without DC voltage shifts or long-lasting decreases in gamma oscillations. Our findings reveal for the first time the acute effects of unilateral hippocampal ischemia on ensemble hippocampal neuronal activities.

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Section: Ttc Stainingmentioning

confidence: 79%

Changes in Hippocampal Neuronal Activity During and After Unilateral Selective Hippocampal IschemiaIn Vivo

Barth¹,

Módy²

2011

J. Neurosci.

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“…Sections were incubated with the vital dye, 2% 2,3,5-triphenyltetrazolium chloride (Sigma) for 15 mins at 371C and fixed in 10% formalin. This technique provides quantification of infarction (Tureyen et al, 2004). A masked observer to treatment groups measured the area of infarction and the area of the ischemic hemisphere of each individual brain section using NIH Image 1.62 (Bethesda, MD, USA).…”

Section: Infarct Measurementmentioning

confidence: 99%

Endotoxin Preconditioning Protects against the Cytotoxic Effects of TNFα after Stroke: A Novel Role for TNFα in LPS-Ischemic Tolerance

Rosenzweig

Minami

Lessov

et al. 2007

J Cereb Blood Flow Metab

143

145

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Lipopolysaccharide (LPS) preconditioning provides neuroprotection against subsequent cerebral ischemic injury. Tumor necrosis factor-a (TNFa) is protective in LPS-induced preconditioning yet exacerbates neuronal injury in ischemia. Here, we define dual roles of TNFa in LPS-induced ischemic tolerance in a murine model of stroke and in primary neuronal cultures in vitro, and show that the cytotoxic effects of TNFa are attenuated by LPS preconditioning. We show that LPS preconditioning significantly increases circulating levels of TNFa before middle cerebral artery occlusion in mice and show that TNFa is required to establish subsequent neuroprotection against ischemia, as mice lacking TNFa are not protected from ischemic injury by LPS preconditioning. After stroke, LPS preconditioned mice have a significant reduction in the levels of TNFa (Bthreefold) and the proximal TNFa signaling molecules, neuronal TNF-receptor 1 (TNFR1), and TNFR-associated death domain (TRADD). Soluble TNFR1 (s-TNFR1) levels were significantly increased after stroke in LPS-preconditioned mice (B2.5-fold), which may neutralize the effect of TNFa and reduce TNFamediated injury in ischemia. Importantly, LPS-preconditioned mice show marked resistance to brain injury caused by intracerebral administration of exogenous TNFa after stroke. We establish an in vitro model of LPS preconditioning in primary cortical neuronal cultures and show that LPS preconditioning causes significant protection against injurious TNFa in the setting of ischemia. Our studies suggest that TNFa is a twin-edged sword in the setting of stroke: TNFa upregulation is needed to establish LPS-induced tolerance before ischemia, whereas suppression of TNFa signaling during ischemia confers neuroprotection after LPS preconditioning.

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“…The permanent occlusion of the MCA distal of the lenticulostriatal arteries can be achieved by a ligation of the artery, its transient compression or by permanent coagulation 8,9 . The resulting infarct in this model predominantly affects the neocortex 10 because the occlusion of the MCA in this model is distal to the lenticulostriatal arteries, which supply the basal ganglia.…”

Section: Introductionmentioning

confidence: 99%

Modeling Stroke in Mice: Permanent Coagulation of the Distal Middle Cerebral Artery

Llovera

Roth

Plesnila

et al. 2014

JoVE

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Stroke is the third most common cause of death and a main cause of acquired adult disability in developed countries. Only very limited therapeutical options are available for a small proportion of stroke patients in the acute phase. Current research is intensively searching for novel therapeutic strategies and is increasingly focusing on the sub-acute and chronic phase after stroke because more patients might be eligible for therapeutic interventions in a prolonged time window. These delayed mechanisms include important pathophysiological pathways such as poststroke inflammation, angiogenesis, neuronal plasticity and regeneration. In order to analyze these mechanisms and to subsequently evaluate novel drug targets, experimental stroke models with clinical relevance, low mortality and high reproducibility are sought after. Moreover, mice are the smallest mammals in which a focal stroke lesion can be induced and for which a broad spectrum of transgenic models are available. Therefore, we describe here the mouse model of transcranial, permanent coagulation of the middle cerebral artery via electrocoagulation distal of the lenticulostriatal arteries, the so-called "coagulation model". The resulting infarct in this model is located mainly in the cortex; the relative infarct volume in relation to brain size corresponds to the majority of human strokes. Moreover, the model fulfills the above-mentioned criteria of reproducibility and low mortality. In this video we demonstrate the surgical methods of stroke induction in the "coagulation model" and report histological and functional analysis tools.

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Infarct volume quantification in mouse focal cerebral ischemia: a comparison of triphenyltetrazolium chloride and cresyl violet staining techniques

Cited by 151 publications

References 19 publications

Changes in Hippocampal Neuronal Activity During and After Unilateral Selective Hippocampal IschemiaIn Vivo

Changes in Hippocampal Neuronal Activity During and After Unilateral Selective Hippocampal IschemiaIn Vivo

Endotoxin Preconditioning Protects against the Cytotoxic Effects of TNFα after Stroke: A Novel Role for TNFα in LPS-Ischemic Tolerance

Modeling Stroke in Mice: Permanent Coagulation of the Distal Middle Cerebral Artery

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