scholarly journals ГИСТОЛОГИЧЕСКИЕ НАРУШЕНИЯ В ГИППОКАМПЕ И ТЕМЕННОЙ КОРЕ ГОЛОВНОГО МОЗГА КРЫС ПРИ ТОТАЛЬНОЙ ЦЕРЕБРАЛЬНОЙ ИШЕМИИ

2020 ◽  
Vol 18 (5) ◽  
pp. 550-555
Author(s):  
E. I. Bon ◽  
◽  
S. M. Zimatkin ◽  
N. Ye. Maksimovich ◽  
K. E. Bashlakova ◽  
...  

Objective. To analyze the changes in the size and shape of perikaryons and the degree of cytoplasm chromatophilia of the rat hippocampal and parietal cortex neurons at different periods after the modeling of total cerebral ischemia. Material and Methods. The experiments were performed on 42 male outbred white rats with an initial weight of 240 ± 20 g. Total cerebral ischemia in white outbred rats was modeled by decapitation. The material for further histological examination was taken at the 1st, 5th, 15th, 30th and 60th minutes, as well as 5 and 24 hours after decapitation. The study of histological preparations was carried out using an Axioscop 2 plus microscope, a digital video camera and the ImageWarp image analysis program. Among the total number, the cells were isolated by the intensity of cytoplasm staining (chromatophilia). After a preliminary check for the normal distribution of indicators, the data obtained were analyzed by non-parametric statistics. Results. With total cerebral ischemia, a decrease in the size of neurons and deformation of perikaryons were observed. Normochromic neurons completely disappeared at the 60th minute. The number of hyperchromic neurons increased, and then progressively decreased. Shrunken neurons made up the majority of cells in the studied cortical sections at the 30–60th minutes, and then, after 5 and 24 hours, cells with pericellular edema prevailed in the neuron population.Conclusion. The obtained data on histological changes in neurons of phylogenetically different parts of the cerebral cortex in the dynamics of total cerebral ischemia provide the basis for further detailed study of post-mortem changes of the brain as well as determining the time of death, thus creating a fundamental basis for studying the properties of neurons, including their transition from one functional state to another.

Author(s):  
Amteshwar Singh Jaggi

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.


2001 ◽  
Vol 1 (6) ◽  
pp. 483-495 ◽  
Author(s):  
Bentham Science Publisher Philip K. Liu

Author(s):  
Shengyuan Wang ◽  
Chuanling Wang ◽  
Lihua Wang ◽  
Zhiyou Cai

Background: Mammalian target of rapamycin (mTOR) has been evidenced as a multimodal therapy in the path-ophysiological process of acute ischemic stroke (AIS). However, the pathway that minocycline targets mTOR signaling is not fully defined in the AIS pathogenesis. This study is to aim at the effects of minocycline on the mTOR signaling in the AIS process and further discover the underlying mechanisms of minocycline involved in the following change of mTOR signaling-autophagy. Methods: Cerebral ischemia/reperfusion (CIR) rat animal models were established with the transient suture occlusion into middle cerebral artery. Minocycline (50mg/kg) was given by intragastric administration. The Morris water maze was used to test the cognitive function of animals. Immunohistochemistry and immunofluorescence were introduced for testing the lev-els of synaptophysin and PSD-95. Western blot was conducted for investigating the levels of mTOR, p-mTOR (Ser2448), p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366), p-eIF4B (Ser406), LC3, p62, synaptophysin and PSD-95. Results: Minocycline prevents cognitive decline of the MCAO stroke rats. Minocycline limits the expression of p-mTOR (Ser2448) and the downstream targets of mTOR [p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366) and p-eIF4B (Ser406)] (P<0.01), while minocycline has no influence on mTOR. LC3-II abundance and the LC3-II/I ratio were upregu-lated in the hippocampus of the MCAO stroke rats by the minocycline therapy (P<0.01). p62 was downregulated in the hippocampus from the MCAO stroke rats administrated with minocycline therapy(P<0.01). The levels of SYP and PSD-95 were up-regulated in the brain of the MCAO stroke rats administrated with minocycline therapy. Conclusion: Minocycline prevents cognitive deficits via inhibiting mTOR signaling and enhancing autophagy process, and promoting the expression of pre-and postsynaptic proteins (synaptophysin and PSD-95) in the brain of the MCAO stroke rats. The potential neuroprotective role of minocycline in the process of cerebral ischemia may be related to mitigating is-chemia-induced synapse injury via inhibiting activation of mTOR signaling.


1917 ◽  
Vol 25 (4) ◽  
pp. 557-580 ◽  
Author(s):  
Carroll G. Bull

Streptococci cultivated from the tonsils of thirty-two cases of poliomyelitis were used to inoculate various laboratory animals. In no case was a condition induced resembling poliomyelitis clinically or pathologically in guinea pigs, dogs, cats, rabbits, or monkeys. On the other hand, a considerable percentage of the rabbits and a smaller percentage of some of the other animals developed lesions due to streptococci. These lesions consisted of meningitis, meningo-encephalitis, abscess of the brain, arthritis, tenosynovitis, myositis, abscess of the kidney, endocarditis, pericarditis, and neuritis. No distinction in the character or frequency of the lesions could be determined between the streptococci derived from poliomyelitic patients and from other sources. Streptococci isolated from the poliomyelitic brain and spinal cord of monkeys which succumbed to inoculation with the filtered virus failed to induce in monkeys any paralysis or the characteristic histological changes of poliomyelitis. These streptococci are regarded as secondary bacterial invaders of the nervous organs. Monkeys which have recovered from infection with streptococci derived from cases of poliomyelitis are not protected from infection with the filtered virus, and their blood does not neutralize the filtered virus in vitro. We have failed to detect any etiologic or pathologic relationship between streptococci and epidemic poliomyelitis in man or true experimental poliomyelitis in the monkey.


2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Jinatta Jittiwat ◽  
Terdthai Tongun ◽  
Supaporn Muchimapura ◽  
Kornkanok Ingkaninan

Cerebral ischemia is known to produce brain damage and related behavioral deficits including memory. Recently, accumulating lines of evidence showed that dietary enrichment with nutritional antioxidants could reduce brain damage and improve cognitive function. In this study, possible protective effect ofZingiber officinale, a medicinal plant reputed for neuroprotective effect against oxidative stress-related brain damage, on brain damage and memory deficit induced by focal cerebral ischemia was elucidated. Male adult Wistar rats were administrated an alcoholic extract of ginger rhizome orally 14 days before and 21 days after the permanent occlusion of right middle cerebral artery (MCAO). Cognitive function assessment was performed at 7, 14, and 21 days after MCAO using the Morris water maze test. The brain infarct volume and density of neurons in hippocampus were also determined. Furthermore, the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in cerebral cortex, striatum, and hippocampus was also quantified at the end of experiment. The results showed that cognitive function and neurons density in hippocampus of rats receiving ginger rhizome extract were improved while the brain infarct volume was decreased. The cognitive enhancing effect and neuroprotective effect occurred partly via the antioxidant activity of the extract. In conclusion, our study demonstrated the beneficial effect of ginger rhizome to protect against focal cerebral ischemia.


2021 ◽  
pp. 58-62
Author(s):  
G. V. Zyrina ◽  
T. A. Slyusa

The purpose of the study. To study clinical and neuroimaging features of chronic cerebral ischemia (CCI) in polycythemia vera (PV).Materials and methods. 66 patients with PV were examined – the main group (43 men, 23 women; mean age 62.0 ± 3.4 years), of which 64 (97.0%) patients were diagnosed with CCI. The comparison group consisted of 85 patients with CCI (34 men, 51 women; mean age 67.7 ± 4.6 years), who developed against the background of cerebral vascular atherosclerosis and arterial hypertension. To identify cognitive disorders, we used Mini Mental State Examination (MMSE). Insomnia was studied in accordance with the criteria of the International Classification of Sleep ICDS‑22005. The quality of sleep was determined using a questionnaire from the Federal Somnological Center. Neuroimaging (MRI of the brain) was performed on Siemens Symphony 1.5 T and GE Signa 1.5 T tomographs.Results. Subjective symptoms CCI are characterized by a greater representation of asthenic and insomniac disorders. Transient ischemic attacks in patients with PV are significantly more common than in the comparison group, their frequency depends on the duration of PV. The revealed changes in MRI of the brain in the majority of PV patients with CCI are characteristic of multiinfarction vascular encephalopathy; in the comparison group, changes that characteristic for subcortical arteriosclerotic encephalopathy were more often recorded.


2021 ◽  
Vol 23 (1) ◽  
pp. 35-38
Author(s):  
L. I. Bon ◽  
◽  
S. M. Zimatkin ◽  

The aim of this work was to study the ultrastructure of the internal pyramidal neurons of the neocortex of 5-day-old rat pups after antenatal alcoholization. The studies were carried out on female outbred white rats with an initial weight of 230 ± 20 g and their offspring. Prenatal alcoholization causes deep and varied ultrastructural changes in pyramidal neurons in the neocortex of 5-day-old rats. Moreover, these violations of direct action not only as a consequence of the damaging effect of alcohol, its metabolite acetehyde or the oxidative stress they cause on the membranes and organelles of neurons during embryogenesis, but also as a violation of the normal "program" of development" of neurons in the cortex.


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