Rat middle cerebral artery occlusion: use of evoked potentials and Tetrazolium staining to assess chronic ischaemia

Lye, R. H.; Shrewsbury-Gee, J.; Slater, P.; Latham, A.

doi:10.1016/0165-0270(87)90007-0

Cited by 18 publications

(6 citation statements)

References 32 publications

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“…TTC has been used for more than 30 years to detect ischaemic damage in a variety of mammalian tissues (Sandritter & Jestadt, 1958). It has been used extensively to stain myocardial tissue from humans and experimental animals and is gaining wider acceptance as a stain in experimental models of cerebral infarction because it is quicker and cheaper to use than conventional histopathology (Liszczak et al, 1984;Bederson et af., 1986;Lundy et al, 1986;Lye et al, 1987). It has been suggested that TTC may be perfused to delineate areas of cerebral ischaemia as early as 4 h after permanent middle cerebral artery occlusion (Park et al, 1988).…”

Section: R H Hatfieid Et Almentioning

confidence: 99%

Triphenyltetrazolium chloride (TTC) as a marker for ischaemic changes in rat brain following permanent middle cerebral artery occlusion

Hatfield

Mendelow

Perry

et al. 1991

Neuropathology Appl Neurobio

107

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Triphenyltetrazolium chloride (TTC) was used to delineate ischaemic lesions in the rat brain at various times following middle cerebral artery occlusion. A comparison was made of TTC staining by immersion and perfusion techniques and conventional light microscopy. The lesions were quantified by measuring the ischaemic area at the sections corresponding to 7 mm in front of the AO line (atlas of Konig and Klippel). In animals examined 24 h after middle cerebral artery occlusion (MCAO), the area of infarction was 17.4 +/- 1.3 mm2 on the TTC perfused slices and 17.6 +/- 1.6 mm2 on the TTC immersed slices (mean +/- SEM). By contrast, there was a marked difference between the two TTC methods when tissues were examined at shorter intervals after artery occlusion. In the TTC-perfused animals, there was no significant difference between the mean areas of infarction measured at 5-20 min, 3-4 h, or 24 h post occlusion. Immersion in TTC, however, failed to reveal any consistent ischaemic damage when applied at the earlier post-occlusion times. Conventional histopathology demonstrated minimal lesions at 5-20 min but at 4 h or more the lesions were not significantly different from those demonstrated by TTC perfusion. TTC immersion staining can, thus, only be used as a reliable marker of cerebral ischaemia damage with post-occlusion survival periods of 24 h. TTC perfusion staining gives results not significantly different from histopathology at 4 h or more post-occlusion but at earlier intervals than 24 h it differs significantly from TTC immersion staining.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: R H Hatfieid Et Almentioning

confidence: 99%

Triphenyltetrazolium chloride (TTC) as a marker for ischaemic changes in rat brain following permanent middle cerebral artery occlusion

Hatfield

Mendelow

Perry

et al. 1991

Neuropathology Appl Neurobio

107

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“…In acute ischemic insults, Glu causes irreversible neuronal damage, which is generally observed at the histological level by the presence of a cortical infarction, and at the electrophysiological level by the correlated loss of somatosensory evoked potentials (SEPs) (Lye et al 1987), cortical disinhibition (Farkas et al 2003), and peri-infarct depolarizations (Mies et al 1993). Since the most of the functional consequences of ischemia can be blocked by the administration of Glu receptor antagonists (Bordi et al 1997;Molchanova et al 2004), one can expect that the elimination of the excess Glu present in the brain interstitial fluids upon ischemia will be of beneficial value.…”

Section: Introductionmentioning

confidence: 99%

Oxaloacetate Decreases the Infarct Size and Attenuates the Reduction in Evoked Responses after Photothrombotic Focal Ischemia in the Rat Cortex

et al. 2009

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A traumatic brain injury or a focal brain lesion is followed by acute excitotoxicity caused by the presence of abnormally high glutamate (Glu) levels in the cerebrospinal and interstitial fluids. It has recently been demonstrated that this excess Glu in the brain can be eliminated into the blood following the intravenous administration of oxaloacetate (OxAc), which, by scavenging the blood Glu, induces an enhanced and neuroprotective brain-to-blood Glu efflux. In this study, we subjected rats to a photothrombotic lesion and treated them after the illumination with a single 30-min-long administration of OxAc (1.2 mg/100 g, i.v.). Following induction of the lesion, we measured the infarct size and the amplitudes of the somatosensory evoked potentials (SEPs) as recorded from the skull surface. The photothrombotic lesion resulted in appreciably decreased amplitudes of the evoked potentials, but OxAc administration significantly attenuated this reduction, and also the infarct size assessed histologically. We suggest that the neuroprotective effects of OxAc are due to its blood Glu-scavenging activity, which, by increasing the brain-to-blood Glu efflux, reduces the excess Glu responsible for the anatomical and functional correlates of the ischemia, as evaluated by electrophysiological evoked potential (EP) measurements.

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“…Neurons in V were stimulated by presenting the lightly-anesthetized rat's right eye with a sinusoidal grating moving in eight different directions, as was used multiple times previously to characterize visual cortical neurons in mice [17,20,21,[47][48][49]. S1 and M1 neurons were stimulated by inserting a thin needle electrode to activate the rat median or sciatic nerves [50,51]. In order to increase the number of simultaneously-recorded cells, we used a 10x 0.5 NA objective to cover 500x500 µm 2 with 512x512 pixels.…”

Section: Recording Single-cell Activity From Multiple Cortical Regionsmentioning

confidence: 99%

Cellular-resolution monitoring of ischemic stroke pathologies in the rat cortex

Chornyy

Das

Borovicka

et al. 2021

Preprint

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Stroke is a leading cause of disability in the Western world. Current post-stroke rehabilitation treatments are only effective in approximately half of the patients. Therefore, there is a pressing clinical need for developing new rehabilitation approaches for enhancing the recovery process, which requires the use of appropriate animal models. Here we study the activity patterns of multiple cortical regions in the rat brain using two-photon microscopy. We longitudinally recorded the fluorescence signal from thousands of neurons labeled with a genetically-encoded calcium indicator before and after an ischemic stroke injury, and found substantial functional changes across motor, somatosensory, and visual cortical regions during the post-stroke cortical reorganization period. We show that a stroke injury in the primary motor cortex has an effect on the activity patterns of neurons not only in the motor and somatosensory cortices, but also in the more distant visual cortex, and that these changes include modified firing rates and kinetics of neuronal activity patterns in response to a sensory stimulus. Changes in neuronal population activity provided animal-specific, circuit-level information on the post-stroke cortical reorganization process, which may be essential for evaluating the efficacy of new approaches for enhancing the recovery process.

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Rat middle cerebral artery occlusion: use of evoked potentials and Tetrazolium staining to assess chronic ischaemia

Cited by 18 publications

References 32 publications

Triphenyltetrazolium chloride (TTC) as a marker for ischaemic changes in rat brain following permanent middle cerebral artery occlusion

Triphenyltetrazolium chloride (TTC) as a marker for ischaemic changes in rat brain following permanent middle cerebral artery occlusion

Oxaloacetate Decreases the Infarct Size and Attenuates the Reduction in Evoked Responses after Photothrombotic Focal Ischemia in the Rat Cortex

Cellular-resolution monitoring of ischemic stroke pathologies in the rat cortex

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