In Vivo Studies of Extracellular Metabolites in the Striatum After Distal Middle Cerebral Artery Occlusion in Stroke-Prone Spontaneously Hypertensive Rats

Shirotani, Toshiki; Shima, Katsuji; Chigasaki, Hiroo

doi:10.1161/01.str.26.5.878

Cited by 7 publications

(7 citation statements)

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“…30 Moreover, in the present study the extracellular concentrations of glutamate and aspartate are 3-fold lower and those of GABA and taurine 10-fold lower than they are 2 hours after probe implantation. 31 The increase in amino acid transmitters and adenosine found in our experiments confirms the increase observed by several authors in both the cortex 17,19 -21,32 and striatum 17,18,22 of anesthetized animals after MCAO. In agreement with them, we found that GABA shows the largest outflow increase of the amino acids.…”

Section: Advantages Of the Intraluminal Approach Of Mcao In Combinatisupporting

confidence: 90%

“…A different factor may be an increase in glutamate metabolism by astrocytes, observed after ischemia in vivo. 49 Unlike the excitatory amino acids, the levels of the inhibitory amino acids GABA and taurine remained high after permanent MCAO, in agreement with the results of Shirotani et al, 22 and are still high 4 hours after MCAO. Two mechanisms may be invoked to explain the long-lasting increase in GABA levels.…”

Section: Neurotransmitter Changes After Mcaosupporting

confidence: 86%

“…13 Furthermore, preischemic administration of A 3 adenosine agonist was shown to impair postischemic blood flow and to enhance mortality and neuronal damage, while an A 3 antagonist was shown to reverse the effects of the agonist in a global ischemia model. 14,15 In this study, using the brain microdialysis technique, we investigated the efflux of excitatory amino acids, ␥-aminobutyric acid (GABA), taurine, and adenosine during permanent focal ischemia induced by the intraluminal MCAO method developed by Zea Longa et al 16 Although several researchers [17][18][19][20][21][22] have investigated the release of amino acids and purines on anesthetized animals after inducing MCAO through a craniectomy, this has not yet been done after MCAO induced by the intraluminal suture technique, 16 a much less invasive method. In this study transmitter level estimations were performed in awake and freely moving animals.…”

Section: See Editorial Comment Page 2455mentioning

confidence: 99%

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Striatal Outflow of Adenosine, Excitatory Amino Acids, γ-Aminobutyric Acid, and Taurine in Awake Freely Moving Rats After Middle Cerebral Artery Occlusion

Melani

Pantoni

Corsi

et al. 1999

Stroke

136

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Background and Purpose-While a number of studies have investigated transmitter outflow in anesthetized animals after middle cerebral artery occlusion (MCAO) performed by craniectomy, studies have never been performed after MCAO induced by intraluminal filament. In addition, it has been reported that after MCAO, infarct volume correlates with functional outcome and with transmitter outflow, although there are no studies that demonstrate a direct correlation between transmitter outflow and functional outcome. The purpose of the present study was to assess excitatory amino acids, ␥-aminobutyric acid, taurine, and adenosine outflow in awake rats after intraluminal MCAO and to determine whether, in the same animal, outflow was correlated with neurological outcome and histological damage. Methods-Vertical microdialysis probes were placed in the striatum of male Wistar rats. After 24 hours, permanent MCAO was induced by the intraluminal suture technique. The transmitter concentrations in the dialysate were determined by high-performance liquid chromatography. Twenty-four hours after MCAO, neurological deficit and histological outcome were evaluated. Results-All transmitters significantly increased after MCAO. Twenty-four hours after MCAO, the rats showed a severe sensorimotor deficit and massive ischemic damage in the striatum and in the cortex (9Ϯ2% and 25Ϯ6% of hemispheric volume, respectively). Significant correlations were found between the efflux of all transmitters, neurological score, and striatal infarct volume. Conclusions-In this study, for the first time, amino acid and adenosine extracellular concentrations during MCAO by the intraluminal suture technique were determined in awake and freely moving rats, and a significant correlation was found between transmitter outflow and neurological deficit. The evaluation of neurological deficit, histological damage, and transmitter outflow in the same animal may represent a useful approach for studying neuroprotective properties of new drugs/agents against focal ischemia. (Stroke. 1999;30:2448-2455.)

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Section: Advantages Of the Intraluminal Approach Of Mcao In Combinatisupporting

confidence: 90%

Section: Neurotransmitter Changes After Mcaosupporting

confidence: 86%

Section: See Editorial Comment Page 2455mentioning

confidence: 99%

See 1 more Smart Citation

Striatal Outflow of Adenosine, Excitatory Amino Acids, γ-Aminobutyric Acid, and Taurine in Awake Freely Moving Rats After Middle Cerebral Artery Occlusion

Melani

Pantoni

Corsi

et al. 1999

Stroke

136

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“…The permanent MCA ligation method which is also referred as pMCAo in the literature is used extensively as a focal ischemia model in rodents [1][2][3][4][5][6] . This method was originally described for rats by Tamura et al in 1981 7 .…”

Section: Introductionmentioning

confidence: 99%

“…Due to the clinical significance there has been a prolonged effort to develop suitable animal models to study the events that unfold during ischemic insult. These techniques include transient or permanent, focal or global ischemia models using many different animal models, with the most common being rodents.The permanent MCA ligation method which is also referred as pMCAo in the literature is used extensively as a focal ischemia model in rodents [1][2][3][4][5][6] . This method was originally described for rats by Tamura et al in 1981 7 .…”

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confidence: 99%

The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse

Colak

Filiano

Johnson

2011

JoVE

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Focal cerebral ischemia is among the most common type of stroke seen in patients. Due to the clinical significance there has been a prolonged effort to develop suitable animal models to study the events that unfold during ischemic insult. These techniques include transient or permanent, focal or global ischemia models using many different animal models, with the most common being rodents.The permanent MCA ligation method which is also referred as pMCAo in the literature is used extensively as a focal ischemia model in rodents [1][2][3][4][5][6] . This method was originally described for rats by Tamura et al. in 1981 7 . In this protocol a craniotomy was used to access the MCA and the proximal regions were occluded by electrocoagulation. The infarcts involve mostly cortical and sometimes striatal regions depending on the location of the occlusion. This technique is now well established and used in many laboratories [8][9][10][11][12][13] . Early use of this technique led to the definition and description of "infarct core" and "penumbra" [14][15][16] , and it is often used to evaluate potential neuroprotective compounds 10,12,13, 17 . Although the initial studies were performed in rats, permanent MCA ligation has been used successfully in mice with slight modifications 18-20 .This model yields reproducible infarcts and increased post-survival rates. Approximately 80% of the ischemic strokes in humans happen in the MCA area 21 and thus this is a very relevant model for stroke studies. Currently, there is a paucity of effective treatments available to stroke patients, and thus there is a need for good models to test potential pharmacological compounds and evaluate physiological outcomes. This method can also be used for studying intracellular hypoxia response mechanisms in vivo.Here, we present the MCA ligation surgery in a C57/BL6 mouse. We describe the pre-surgical preparation, MCA ligation surgery and 2,3,5 Triphenyltetrazolium chloride (TTC) staining for quantification of infarct volumes. ProtocolThis protocol was approved by the University of Rochester committee devoted to the ethical use of animals in research (UCAR). Aseptic techniques should be followed during the protocol. The use of sterile gloves and a mask is required.All the equipment, materials, chemicals, and tools that are used during the protocol are described in Table 1. Pre-surgical Preparation Surgical Procedure and MCA LigationPage 1 of 4 Journal of Visualized Experiments www.jove.comCopyright © 2011 Journal of Visualized Experiments 1. Inject mice subcutaneously with buprenorphine (0.05mg/kg) 2 h before surgery, immediately after the surgery and then every 3-5 h during the first 24 h post-operative period. 2. Sterilize all the surgical instruments, gauze sponges, and cotton tip applicators by autoclave. Keep surgical tools in 70% ethanol during the surgery and air dry on sterile gauze right before use. Spray the work area with 70% ethanol. 3. Anesthetize the mouse with a 3% isofluorane-20% oxygen gas mixture by using an anesthetic vap...

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Time-course of protection by the selective A2A receptor antagonist SCH58261 after transient focal cerebral ischemia

et al. 2015

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Evidence indicates that the adenosine A2A receptor subtype is of critical importance in stroke. In previous studies, in the model of permanent middle cerebral artery occlusion (pMCAo), the adenosine A2A receptor antagonist, SCH58261, administered soon after ischemia, proved protective against excessive glutamate outflow in the first 4 h after ischemia and against neurological deficit and tissue damage evaluated 24 h after pMCAo. In the present work, we investigated if neuroprotective effect of SCH58261 was maintained 7 days after transient MCAo (tMCAo). SCH58261 (0.01 mg/kg, i.p.), administered twice/day for 7 days, protected from neurological deficit 1 day after tMCAo, but no more after 5 and 7 days. Two days after tMCAo, SCH58261 did not reduce blood cell infiltration, evaluated as HIS-48 positive cells, into ischemic striatal and cortical tissue. Moreover, 7 days after tMCAo, SCH58261 has not protected ischemic areas from damage and has not ameliorated myelin organization into the ischemic striatum. Protection by the A2A receptor antagonist 24 h after ischemia is attributable to reduced excitotoxicity. Seven days after ischemia the early protective effect of the A2A receptor antagonist likely has been overwhelmed by a secondary damage due to blood cell infiltration and neuroinflammation.

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In Vivo Studies of Extracellular Metabolites in the Striatum After Distal Middle Cerebral Artery Occlusion in Stroke-Prone Spontaneously Hypertensive Rats

Cited by 7 publications

References 38 publications

Striatal Outflow of Adenosine, Excitatory Amino Acids, γ-Aminobutyric Acid, and Taurine in Awake Freely Moving Rats After Middle Cerebral Artery Occlusion

Striatal Outflow of Adenosine, Excitatory Amino Acids, γ-Aminobutyric Acid, and Taurine in Awake Freely Moving Rats After Middle Cerebral Artery Occlusion

The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse

Time-course of protection by the selective A2A receptor antagonist SCH58261 after transient focal cerebral ischemia

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