Different Mechanisms of Secondary Neuronal Damage in Thalamic Nuclei After Focal Cerebral Ischemia in Rats

We examined whether Brazilian green propolis, a widely used folk medicine, has a neuroprotective functionin vitroand/orin vivo.In vitro, propolis significantly inhibited neurotoxicity induced in neuronally differentiated PC12 cell cultures by either 24 h hydrogen peroxide (H2O2) exposure or 48 h serum deprivation. Regarding the possible underlying mechanism, propolis protected against oxidative stress (lipid peroxidation) in mouse forebrain homogenates and scavenged free radicals [induced by diphenyl-p-picrylhydrazyl (DPPH). In micein vivo, propolis [30 or 100 mg/kg; intraperitoneally administered four times (at 2 days, 1 day and 60 min before, and at 4 h after induction of focal cerebral ischemia by permanent middle cerebral artery occlusion)] reduced brain infarction at 24 h after the occlusion. Thus, a propolis-induced inhibition of oxidative stress may be partly responsible for its neuroprotective function againstin vitrocell death andin vivofocal cerebral ischemia.

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Antisense Knockdown of the Glial Glutamate Transporter GLT-1, But Not the Neuronal Glutamate Transporter EAAC1, Exacerbates Transient Focal Cerebral Ischemia-Induced Neuronal Damage in Rat Brain

Journal of Neuroscience ◽

10.1523/jneurosci.21-06-01876.2001 ◽

2001 ◽

Vol 21 (6) ◽

pp. 1876-1883 ◽

Cited By ~ 162

Author(s):

Vemuganti L. Raghavendra Rao ◽

Aclan Dogan ◽

Kathryn G. Todd ◽

Kellie K. Bowen ◽

Bum-Tae Kim ◽

...

Keyword(s):

Cerebral Ischemia ◽

Rat Brain ◽

Neuronal Damage ◽

Focal Cerebral Ischemia ◽

Glutamate Transporter ◽

Glial Glutamate Transporter ◽

Transient Focal Cerebral Ischemia ◽

Antisense Knockdown ◽

Neuronal Glutamate Transporter

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Temperature Modulation of Cerebral Depolarization during Focal Cerebral Ischemia in Rats: Correlation with Ischemic Injury

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1993.52 ◽

1993 ◽

Vol 13 (3) ◽

pp. 389-394 ◽

Cited By ~ 159

Author(s):

Qun Chen ◽

Michael Chopp ◽

Gordon Bodzin ◽

Hua Chen

Keyword(s):

Cerebral Ischemia ◽

Neuronal Damage ◽

Focal Cerebral Ischemia ◽

Cell Damage ◽

Infarct Volume ◽

Cortical Lesion ◽

Temperature Modulation ◽

Ischemic Infarct ◽

Dc Potential ◽

Ischemic Depolarization

The role of cerebral depolarizations in focal cerebral ischemia is unknown. We therefore measured the direct current (DC) electrical activity in the cortex of Wistar rats subjected to transient occlusion of the middle cerebral artery (MCA). Focal ischemia was induced for 90 min by insertion of an intraluminal filament to occlude the MCA. To modulate cell damage, we subjected the rats to hypothermic (30°C, n = 4), normothermic (37°C, n = 4), and hyperthermic (40°C, n = 6) ischemia. Controlled temperatures were also maintained during 1 h of reperfusion. Continuous cortical DC potential changes were measured using two active Ag–AgCl electrodes placed in the cortical lesion. Animals were killed 1 week after ischemia. The brains were sectioned and stained with hematoxylin and eosin, for evaluation of neuronal damage, and calculation of infarct volume. All animals exhibited an initial depolarization within 30 min of ischemia, followed by a single depolarization event in hypothermic animals, and multiple periodic depolarization events in both normothermic and hyperthermic animals. Hyperthermic animals exhibited significantly more (p < 0.05) DC potential deflections (n = 6.17 ± 0.67) than normothermic animals (n = 2.75 ± 0.96). The ischemic infarct volume (% of hemisphere) was significantly different for the various groups; hypothermic animals exhibited no measurable infarct volume, while the ischemic infarct volume was 10.2 ± 12.3% in normothermic animals and 36.5 ± 3.4% in hyperthermic animals (p < 0.05). A significant correlation was detected between the volume of infarct and number of depolarization events ( r = 0.90, p < 0.001). Our data indicate that body temperature has a profound effect on the number of ischemic depolarization events, and ischemic cell damage after transient MCA occlusion, and suggest a role for ischemic depolarizations in mediating ischemic cell damage.

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SMI-32 — a novel axonal injury marker for investigation of ischemic brain pathology

Medical academic journal ◽

10.17816/maj49849 ◽

2021 ◽

Vol 20 (4) ◽

pp. 63-68

Author(s):

Daria L. Tsyba ◽

Olga V. Kirik ◽

Dmitrii E. Korzhevskii

Keyword(s):

Cerebral Ischemia ◽

Heavy Chain ◽

Neuronal Damage ◽

Focal Cerebral Ischemia ◽

Axonal Injury ◽

Experimental Models ◽

Nerve Fibers ◽

Left Middle Cerebral Artery ◽

Social Significance ◽

Neurofilament Proteins

The relevance of this work is determined by the high prevalence and social significance of cerebrovascular diseases and the need to develop effective methods for verifying neuronal damage due to cerebral ischemia in experimental models. The aim of this study was to assess the possibility of immunohistochemical revealing of neurofilaments to detect axonal injury in cerebral ischemia models. Materials and methods. A model of transient focal cerebral ischemia by the left middle cerebral artery occlusion was reproduced in male Wistar, SHR and WKY rats. Axonal injury was assessed by immunohistochemical reactions for neurofilament proteins using SMI-32 and 2F11 antibodies. Results. In cerebral ischemia, damage to nerve fibers occurs, manifested by thickening of axons, their varicose expansion and segmental accumulation of neurofilament proteins. These changes are more noticeable with an immunohistochemical reaction to the SMI-32 marker of neurofilament heavy chain. Conclusions. The use of antibodies to the non-phosphorylated neurofilament heavy chain makes it easy to identify degenerating nerve fibers and can be recommended as an alternative method for detecting axonal injury.

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