scholarly journals PECULIARITIES OF MORPHOLOGICAL CHANGES IN BRAIN STRUCTURES OF RATS UNDER CONDITIONS OF MODEL TRAUMATIC BRAIN INJURY

2021 ◽  
Vol 20 (2) ◽  
Author(s):  
S.I. Semenenko

Experimental animal models of traumatic brain injury (TBI) were created to study themorpho-functional features of the disease and to fill the therapeutic window betweenpreclinical trials and the introduction of drugs into the clinical medical practice.The aim of the work – to study the morphological changes in the brain structures ofrats under conditions of model TBI.Material and methods. The experiments were performed on white male rats weighing160-190 g. The experimental model of TBI in rats under conditions of propofolanesthesia (60 mg/kg) was caused by the action of a stream of carbon dioxide underpressure, which was created using a gas cylinder air gun. For histological examination,the brain was fixed with 10% neutral formalin, dehydrated in alcohols in increasingconcentrations, and immersed in paraffin. Sections were stained with hematoxylinand eosin, toluidine blue. The microscopy of histological specimens was performedusing a light microscope OLIMPUS BX 41 using magnifications of 40, 100, 200 and400 times. The morphological research studied the structural changes of neurons inthe sensorimotor zone of the cerebral cortex, the hippocampal structures of the CA1zone and the condition of blood vessels in two groups of animals: Group II - rats withsimulated trauma.Results. In animals with model TBI, there was a predominance of the number ofdegenerating pyramidal neurons over those preserved in the sensorimotor zone ofthe cortex of the large hemispheres and in the CA1 zone of the hippocampus. In thesensorimotor zone of the cortex of the large hemispheres, the death of neurons wasmanifested by morphological signs of karyopyknosis, karyorexis and cytopicnosiswith the phenomena of cytolysis. Only single preserved neurons were visualized in thepyramidal layer; most cells are represented by pyknotic cells; 3) in the hippocampusof animals with TBI, the cytolytic type of nerve cell death was mainly observed. Themorphological signs of cytolysis indicate deep damage to all neurocyte structures.Conclusions. The morphological basis of the remodeling of brain structures in traumaticbrain injury is: reduction in the number of normochromic neurons in experimentalanimals, formation of a significant number of hypochromic neurons, formation ofhyperchromic neurons with pronounced signs of tigrolysis, hemodynamic disorderswith pericellular and perivascular edema.

2016 ◽  
Vol 07 (S 01) ◽  
pp. S076-S079 ◽  
Author(s):  
Ashok Munivenkatappa ◽  
Amit Agrawal

ABSTRACTDegree of recovery after traumatic brain injury is highly variable that lasts for many weeks to months. The evidence of brain structures involved in recovery mechanisms is limited. This review highlights evidence of the brain structure particularly thalamus in neuroplasticity mechanism. Thalamus with its complex global networking has potential role in refining the cortical and other brain structures. Thalamic nuclei activation both naturally or by neurorehabilitation in injured brain can enhance and facilitate the improvement of posttraumatic symptoms. This review provides evidence from literature that thalamus plays a key role in recovery mechanism after injury. The study also emphasize that thalamus should be specifically targeted in neurorehabilitation following brain injury.


2020 ◽  
Vol 34 (7) ◽  
pp. 616-626 ◽  
Author(s):  
Yanlu Zhang ◽  
Yi Zhang ◽  
Michael Chopp ◽  
Zheng Gang Zhang ◽  
Asim Mahmood ◽  
...  

Background. Mesenchymal stem cell (MSC)-derived exosomes play a critical role in regenerative medicine. Objective. To determine the dose- and time-dependent efficacy of exosomes for treatment of traumatic brain injury (TBI). Methods. Male rats were subjected to a unilateral moderate cortical contusion. In the dose-response study, animals received a single intravenous injection of exosomes (50, 100, 200 µg per rat) or vehicle, with treatment initiated at 1 day after injury. In the therapeutic window study, animals received a single intravenous injection of 100 µg exosomes or vehicle starting at 1, 4, or 7 days after injury. Neurological functional tests were performed weekly after TBI for 5 weeks. Spatial learning was measured on days 31 to 35 after TBI using the Morris water maze test. Results. Compared with the vehicle, regardless of the dose and delay in treatment, exosome treatment significantly improved sensorimotor and cognitive function, reduced hippocampal neuronal cell loss, promoted angiogenesis and neurogenesis, and reduced neuroinflammation. Exosome treatment at 100 µg per rat exhibited a significant therapeutic effect compared with the 50- or 200-µg exosome groups. The time-dependent exosome treatment data demonstrated that exosome treatment starting at 1 day post-TBI provided a significantly greater improvement in functional and histological outcomes than exosome treatments at the other 2 delayed treatments. Conclusions. These results indicate that exosomes have a wide range of effective doses for treatment of TBI with a therapeutic window of at least 7 days postinjury. Exosomes may provide a novel therapeutic intervention in TBI.


2021 ◽  
Vol 7 (6) ◽  
Author(s):  
M. Shuvalova ◽  
Yu. Shidakov ◽  
A. Shanazarov

Human activity is associated with the risk of injury. The rate of cases of traumatic brain injury (TBI) in high-altitude conditions is high. It should be assumed that exogenous hypoxia will have a significant impact on the development of the clinical consequences of TBI. However, information about the behavior of animals on the background of TBI in the highlands is scarce. The search for means of correcting brain injuries remains an urgent issue. To date, glibenclamide has been proposed for this purpose, but its effect in the highlands has not been studied. Objective: to evaluate the effect of glibenclamide on the behavioral activity of animals with TBI in the highlands. The object of the study is 82 white male rats weighing 250–310 g. The low-mountain series of the experiment was carried out at an altitude of 760 m above sea level (Bishkek). The high-altitude series was modeled on the Tuya-Ashu pass — 3200 m above sea level (Kyrgyzstan). TBI was reproduced according to the method of Y. Tang (1997). Correction with glibenclamide at a dose of 0.1 mg/kg per os. Behavioral activity was evaluated using the Open Field method, and muscle strength was evaluated using the S. V. Speransky method on the 3rd day of the experiment. Statistical processing of the obtained data was carried out in the SPSS 16.0 program. TBI in the low mountains resulted in a decrease in locomotor activity by 67% (P<0.001), and efficiency — by 43% (P<0.001). In the group of rats with TBI in the highlands, compared with the data of healthy animals that visited the same altitude, locomotor activity decreased by 44% (P<0.001), racks — by 60% (P<0.001), minks — by 76% (P< 0.01), grooming — by 55% (P<0.01), the number of boluses of defecation increases by 37% (P<0.05). Correction of TBI with glibenclamide in the highlands led to an increase in locomotion by 2 times (P<0.001), standing — by 2.3 times, peering into minks — by 4 times (P<0.01), working capacity — by 2.04 times (P<0.001). The level of defecation decreased by 70% (P<0.001). Violations of the behavior of rats in the highlands with TBI without the use of glibenclamide are more pronounced than in experiments in the foothills. Correction of TBI that occurred in the highlands demonstrates a positive neurotropic effect of glibenclamide.


2021 ◽  
Vol 8 (4) ◽  
pp. 263-272
Author(s):  
R. F. Cherevatenko ◽  
O. V. Antsiferov ◽  
S. Y. Skachilova ◽  
M. V. Pokrovsky ◽  
V. V. Gureev ◽  
...  

The aim of the study is to search compounds with neuroprotective properties among new ethylthiadiazole derivatives in simulated traumatic brain injury.Materials and methods. The experiment was carried out on 78 white male rats 270±20 g line “Wistar” 5–6 months of age and 120 outbred sexually mature mice weighing 20±2 grams. The article describes the search for compounds with neuroprotective properties among new ethylthiadiazole derivatives under the codes LKHT 4–15, LKHT 10–18, LKHT 11–18, and LKHT 12–18 in experimental traumatic brain injury in rats. Acute toxicity of the compounds was studied. Pharmacological screening was performed using behavioral and neurological research methods. The McGraw stroke score scale modified by I.V. Gannushkina and the mNSS psychometric scale were used in the study. The open field and Rota-rod tests were used to assess the behavioral status of the animals.Results. The compound-LKHT 12–18 at a dose of 50 mg/kg was detected as a leader. In pharmacological correction of pathology, this compound had the lowest percentage of fatality among the studied compounds (8%), the severity of neurological deficit was significantly reduced, the lowest scores and a higher level of motor activity of the limbs were registered. The number of rearing in the group of animals receiving the compound LKHT 12–18 at the dose of 50 mg/kg increased by 1.5 times, statistically significant (p<0.05) in comparison with the control group. Based on the results of the “Rota-rod” test, the total time of holding animals on the rod for 3 attempts was statistically significantly different in the groups administered with LKHT 12–18 derivatives (1.5 times longer) at the dose of 50 mg/kg compared with the control (p<0.05).Conclusion. Based on the results obtained in this study, it is planned to study in more detail the compound LKHT 12–18 at the dose of 50 mg/kg.


2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.


2018 ◽  
pp. 110-119

Primary Objectives: By extending the scope of knowledge of the primary care optometrist, the brain injury population will have expanded access to entry level neurooptometric care by optometric providers who have a basic understanding of their neurovisual problems, be able to provide some treatment and know when to refer to their colleagues who have advanced training in neuro-optometric rehabilitation.


2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.


Author(s):  
Eunyoung Park ◽  
Johnathan G. Lyon ◽  
Melissa Alvarado‐Velez ◽  
Martha I. Betancur ◽  
Nassir Mokarram ◽  
...  

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