A simple novel technique to induce short-lasting local brain ischaemia in the rat

Levente Knapp, Levente Gellért, Judit Herédi, Kitti Kocsis, Gáspár Oláh, János Fuzik, Z. Kis, L. Vécsei, J. Toldi, T. Farkas

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Aims: Brain ischaemia models are essential to study the pathomechanisms of stroke. Our aim was to investigate the reliability and reproducibility of our novel focal ischaemia-reperfusion model. Methods: To induce a cortical transient ischaemic attack, we lifted the distal middle cerebral artery (MCA) with a special hook. The early changes after 2×15-min occlusion were observed in the somatosensory evoked responses (SERs). The histological responses to 2×15-min MCA occlusion and to 30-, 45- or 60-min ischaemia were examined after a 1-day survival period by 2,3,5-triphenyltetrazolium chloride (TTC) and Fluoro Jade C (FJC) staining. Another group, with 30-min ischaemia, was analysed histologically by FJC, S100 and CD11b labelling after a 5-day survival period. Results: The amplitudes of the SERs decreased immediately at the beginning of the ischaemic period, and remained at a reduced level during the ischaemia. Reperfusion resulted in increasing SER amplitudes, but they never regained the control level. The short-lasting ischaemia did not lead to brain infarction when evaluated with TTC, but intense labelling was found with FJC. The 30-min ischaemia did not result in FJC labelling after 1 day, but marked labelling was observed after 5 days with FJC, S100 and CD11b in the cortical area supplied by the MCA. Conclusions: We present here a novel, readily reproducible method to induce focal brain ischaemia. The ischaemia-reperfusion results in noteworthy changes in the SERs and the appearance of conventional tissue damage markers. This method involves possibilities for precise blood flow regulation, and the setting of the required level of perfusion.

Original languageEnglish
Pages (from-to)603-609
Number of pages7
JournalNeuropathology and Applied Neurobiology
Volume40
Issue number5
DOIs
Publication statusPublished - 2014

Fingerprint

Brain Ischemia
Ischemia
Reperfusion
Middle Cerebral Artery
Brain Infarction
Middle Cerebral Artery Infarction
Transient Ischemic Attack
Perfusion
Stroke
fluoro-jade C
Staining and Labeling

Keywords

  • Brain ischaemia
  • Fluoro Jade C
  • Middle cerebral artery occlusion (MCAO)
  • Somatosensory evoked potentials
  • Stroke
  • TIA

ASJC Scopus subject areas

  • Clinical Neurology
  • Pathology and Forensic Medicine
  • Neurology
  • Histology
  • Physiology (medical)
  • Medicine(all)

Cite this

A simple novel technique to induce short-lasting local brain ischaemia in the rat. / Knapp, Levente; Gellért, Levente; Herédi, Judit; Kocsis, Kitti; Oláh, Gáspár; Fuzik, János; Kis, Z.; Vécsei, L.; Toldi, J.; Farkas, T.

In: Neuropathology and Applied Neurobiology, Vol. 40, No. 5, 2014, p. 603-609.

Research output: Contribution to journalArticle

Knapp, Levente ; Gellért, Levente ; Herédi, Judit ; Kocsis, Kitti ; Oláh, Gáspár ; Fuzik, János ; Kis, Z. ; Vécsei, L. ; Toldi, J. ; Farkas, T. / A simple novel technique to induce short-lasting local brain ischaemia in the rat. In: Neuropathology and Applied Neurobiology. 2014 ; Vol. 40, No. 5. pp. 603-609.
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abstract = "Aims: Brain ischaemia models are essential to study the pathomechanisms of stroke. Our aim was to investigate the reliability and reproducibility of our novel focal ischaemia-reperfusion model. Methods: To induce a cortical transient ischaemic attack, we lifted the distal middle cerebral artery (MCA) with a special hook. The early changes after 2×15-min occlusion were observed in the somatosensory evoked responses (SERs). The histological responses to 2×15-min MCA occlusion and to 30-, 45- or 60-min ischaemia were examined after a 1-day survival period by 2,3,5-triphenyltetrazolium chloride (TTC) and Fluoro Jade C (FJC) staining. Another group, with 30-min ischaemia, was analysed histologically by FJC, S100 and CD11b labelling after a 5-day survival period. Results: The amplitudes of the SERs decreased immediately at the beginning of the ischaemic period, and remained at a reduced level during the ischaemia. Reperfusion resulted in increasing SER amplitudes, but they never regained the control level. The short-lasting ischaemia did not lead to brain infarction when evaluated with TTC, but intense labelling was found with FJC. The 30-min ischaemia did not result in FJC labelling after 1 day, but marked labelling was observed after 5 days with FJC, S100 and CD11b in the cortical area supplied by the MCA. Conclusions: We present here a novel, readily reproducible method to induce focal brain ischaemia. The ischaemia-reperfusion results in noteworthy changes in the SERs and the appearance of conventional tissue damage markers. This method involves possibilities for precise blood flow regulation, and the setting of the required level of perfusion.",
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AU - Knapp, Levente

AU - Gellért, Levente

AU - Herédi, Judit

AU - Kocsis, Kitti

AU - Oláh, Gáspár

AU - Fuzik, János

AU - Kis, Z.

AU - Vécsei, L.

AU - Toldi, J.

AU - Farkas, T.

PY - 2014

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N2 - Aims: Brain ischaemia models are essential to study the pathomechanisms of stroke. Our aim was to investigate the reliability and reproducibility of our novel focal ischaemia-reperfusion model. Methods: To induce a cortical transient ischaemic attack, we lifted the distal middle cerebral artery (MCA) with a special hook. The early changes after 2×15-min occlusion were observed in the somatosensory evoked responses (SERs). The histological responses to 2×15-min MCA occlusion and to 30-, 45- or 60-min ischaemia were examined after a 1-day survival period by 2,3,5-triphenyltetrazolium chloride (TTC) and Fluoro Jade C (FJC) staining. Another group, with 30-min ischaemia, was analysed histologically by FJC, S100 and CD11b labelling after a 5-day survival period. Results: The amplitudes of the SERs decreased immediately at the beginning of the ischaemic period, and remained at a reduced level during the ischaemia. Reperfusion resulted in increasing SER amplitudes, but they never regained the control level. The short-lasting ischaemia did not lead to brain infarction when evaluated with TTC, but intense labelling was found with FJC. The 30-min ischaemia did not result in FJC labelling after 1 day, but marked labelling was observed after 5 days with FJC, S100 and CD11b in the cortical area supplied by the MCA. Conclusions: We present here a novel, readily reproducible method to induce focal brain ischaemia. The ischaemia-reperfusion results in noteworthy changes in the SERs and the appearance of conventional tissue damage markers. This method involves possibilities for precise blood flow regulation, and the setting of the required level of perfusion.

AB - Aims: Brain ischaemia models are essential to study the pathomechanisms of stroke. Our aim was to investigate the reliability and reproducibility of our novel focal ischaemia-reperfusion model. Methods: To induce a cortical transient ischaemic attack, we lifted the distal middle cerebral artery (MCA) with a special hook. The early changes after 2×15-min occlusion were observed in the somatosensory evoked responses (SERs). The histological responses to 2×15-min MCA occlusion and to 30-, 45- or 60-min ischaemia were examined after a 1-day survival period by 2,3,5-triphenyltetrazolium chloride (TTC) and Fluoro Jade C (FJC) staining. Another group, with 30-min ischaemia, was analysed histologically by FJC, S100 and CD11b labelling after a 5-day survival period. Results: The amplitudes of the SERs decreased immediately at the beginning of the ischaemic period, and remained at a reduced level during the ischaemia. Reperfusion resulted in increasing SER amplitudes, but they never regained the control level. The short-lasting ischaemia did not lead to brain infarction when evaluated with TTC, but intense labelling was found with FJC. The 30-min ischaemia did not result in FJC labelling after 1 day, but marked labelling was observed after 5 days with FJC, S100 and CD11b in the cortical area supplied by the MCA. Conclusions: We present here a novel, readily reproducible method to induce focal brain ischaemia. The ischaemia-reperfusion results in noteworthy changes in the SERs and the appearance of conventional tissue damage markers. This method involves possibilities for precise blood flow regulation, and the setting of the required level of perfusion.

KW - Brain ischaemia

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KW - Somatosensory evoked potentials

KW - Stroke

KW - TIA

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