TracMouse: A computer aided movement analysis script for the mouse inverted horizontal grid test

Niewiadomski, Wiktor; Pałasz, Ewelina; Skupinska, Malgorzata; Żyliński, Marek; Steczkowska, M; Gąsiorowska, Anna; Niewiadomska, Grażyna; Riedel, Gernot

doi:10.1038/srep39331

Cited by 5 publications

(5 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The inverted grid test was then used by other researchers (57–63), but none of them demonstrated any correlation between motor performance and the degree of dopaminergic neuron loss. Interestingly, in the study that provides an in-depth analysis of many motor parameters (64), no adverse effect of MPTP treatment was noticed.…”

Section: Exercise Induces Recovery Of Motor Function and Neuroprotectmentioning

confidence: 96%

Exercise-Induced Neuroprotection and Recovery of Motor Function in Animal Models of Parkinson's Disease

et al. 2019

View full text Add to dashboard Cite

Parkinson's disease (PD) is manifested by progressive motor, autonomic, and cognitive disturbances. Dopamine (DA) synthesizing neurons in the substantia nigra (SN) degenerate, causing a decline in DA level in the striatum that leads to the characteristic movement disorders. A disease-modifying therapy to arrest PD progression remains unattainable with current pharmacotherapies, most of which cause severe side effects and lose their efficacy with time. For this reason, there is a need to seek new therapies supporting the pharmacological treatment of PD. Motor therapy is recommended for pharmacologically treated PD patients as it alleviates the symptoms. Molecular mechanisms behind the beneficial effects of motor therapy are unknown, nor is it known whether such therapy may be neuroprotective in PD patients. Due to obvious limitations, human studies are unlikely to answer these questions; therefore, the use of animal models of PD seems indispensable. Motor therapy in animal models of PD characterized by the loss of dopaminergic neurons has neuroprotective and neuroregenerative effects, and the completeness of neuronal protection may depend on (i) degree of neuronal loss, (ii) duration and intensity of exercise, and (iii) time elapsed between insult and commencing of training. As the physical activity is neuroprotective for dopaminergic neurons, the question arises what is the mechanism of this protective action. A current hypothesis assumes a central role of neurotrophic factors in the neuroprotection of dopaminergic neurons, even though it is still not clear whether increased DA level in the nigrostriatal axis results from neurogenesis of dopaminergic neurons in the SN, recovery of the phenotype of dopaminergic neurons, increased sprouting of the residual dopaminergic axons in the striatum, or generation of local striatal neurons from inhibitory interneurons. In the present review, we discuss studies describing the influence of physical exercise on the PD-like changes manifested in animal models of the disease and focus our interest on the current state of knowledge on the mechanism of neuroprotection induced by physical activity as a supportive therapy in PD.

show abstract

Section: Exercise Induces Recovery Of Motor Function and Neuroprotectmentioning

confidence: 96%

Exercise-Induced Neuroprotection and Recovery of Motor Function in Animal Models of Parkinson's Disease

et al. 2019

View full text Add to dashboard Cite

show abstract

“…The behavioral evaluation was performed on the 14th day after insult with a horizontal grid test (Niewiadomski W et al 2016) and pole-climbing test (Gao Y et al 2019). The horizontal grid test was designed to evaluate the grasping ability of mouse limbs.…”

Section: Behavioral Testmentioning

confidence: 99%

Human umbilical cord mesenchymal stem cell-derived exosomes improve brain tissue and functional recovery in mice with cerebral palsy

Chen

Sai

Cui

et al. 2023

Preprint

View full text Add to dashboard Cite

Cerebral palsy (CP) is a neurodevelopmental and motor disorder syndrome threatening children’s physical and mental health. Hypoxic-ischemic brain injury and inflammation have been considered as the main causes of CP. Mesenchymal stem cells (MSCs) can repair brain tissue damage, and many studies have proved that exosomes from MSCs have a critical advantage in the central nervous system (CNS) disease. Therefore, this study aimed to explore the improvement effect of human umbilical cord MSC (hUC-MSC)-derived exosomes on CP and whether synergistic action existed when combined with mouse nerve growth factor (mNGF). Therefore, the exosomes were isolated from hUC-MSCs and examined using electron microscopy, particle size, and Western blot (WB). A CP model was constructed by hypoxic induction after unilateral common carotid artery ligation combined with lipopolysaccharide (LPS) infection. The pathological damage of neuron tissue and synaptic structure in the hippocampus was determined using a light microscope after hematoxylin-eosin (HE) staining and transmission electron microscopy, respectively. The survival of neurons was analyzed using Nissl staining. The WB analysis was performed to monitor postsynaptic density 95(PSD-95) and synaptophysin(SYN) protein levels. The results showed that exosomes released by hUC-MSCs could ameliorate the motor function in mice with CP by rescuing the impaired brain tissue, synaptic structure, and neuronal function with increased PSD-95 and SYN levels. When the exosome was combined with mNGF, an improvement in CP was found. The results indicated that the intravenously injected hUC-MSC-exosomes and intraperitoneal administration of mNGF alleviated the nerve function injury in mice with CP.

show abstract

“…Аналогичным образом, дисферлинопатия может прогрессировать с различной скоростью, даже при наличии одной и той же мутации [12,13]. Описан ряд факторов, модифицирующих фенотип и скорость прогрессирования дисферлинопатии: степень и продолжительность физической активности и тип мутации (гомозиготность по нонсенс-мутациям), при отсутствии устойчивых клинико-генетических корреляций [14,15].…”

Section: дисферлинопатияunclassified

В6.А-DYSFPRMD/GENEJ Mice as a Genetic Model of Dysferlinopathy

Корокин

Kuzubova

Radchenko

et al. 2022

Farm. farmakol. (Pâtigorsk)

View full text Add to dashboard Cite

The aim of the work was behavioral and pathomorphological phenotyping of the mice knockout for the DYSF gene, which plays an important role in the development and progression of dysferlinopathy.Materials and methods. A B6.A-Dysfprmd/GeneJ (Bla/J) mice subline was used in the work. During the study, a muscle activity was determined basing on the following tests: “Inverted grid”, “Grip strength”, “Wire Hanging”, “Weight-loaded swimming”, Vertical Pole”. Histological and immunofluorescent examinations of skeletal muscles (m. gastrocnemius, m. tibialis) were performed. The presence and distribution of the dysferlin protein was assessed, and general histological changes in the skeletal muscle characteristics of mice at the age of 12 and 24 weeks, were described. A morphometric analysis with the determination of the following parameters was performed: the proportion of necrotic muscle fibers; the proportion of fibers with centrally located nuclei; the mean muscle fiber diameter.Results. The “Grip strength” test and the “Weight-loaded swimming” test revealed a decrease in the strength of the forelimbs and endurance in the studied mice of the Bla/J subline compared to the control line. The safety of physical performance was checked using the “Wire Hanging” test and the “Vertical Pole” test, which showed a statistically significant difference between the studied mice and control. The coordination of movements and muscle strength of the limbs examined in the “Inverted Grid” test did not change in these age marks. Decreased grip strength of the forelimbs, decreased physical endurance with age, reflects the progression of the underlying muscular disease. Histological methods in the skeletal muscles revealed signs of a myopathic damage pattern: necrotic muscle fibers, moderate lympho-macrophage infiltration, an increase in the proportion of fibers with centrally located nuclei, and an increase in the average fiber diameter compared to the control. The dysferlin protein was not found out in the muscle tissues.Conclusion. Taking into account the results of the tests performed, it was shown that the absence of Dysf-/- gene expressionin Bla/J subline mice led to muscular dystrophy with the onset of the development of phenotypic disease manifestations at the age of 12 weeks and their peak at 24 weeks. Histopathological phenotypic manifestations of the disease are generally nonspecific and corresponded to the data of intravital pathoanatomical examination in diferlinopathy patients. The mice of the studied subline Bla/J are a representative model of dysferlinopathy and can be used to evaluate new therapeutic agents for the treatment of this disease.

show abstract

TracMouse: A computer aided movement analysis script for the mouse inverted horizontal grid test

Cited by 5 publications

References 31 publications

Exercise-Induced Neuroprotection and Recovery of Motor Function in Animal Models of Parkinson's Disease

Exercise-Induced Neuroprotection and Recovery of Motor Function in Animal Models of Parkinson's Disease

Human umbilical cord mesenchymal stem cell-derived exosomes improve brain tissue and functional recovery in mice with cerebral palsy

В6.А-DYSFPRMD/GENEJ Mice as a Genetic Model of Dysferlinopathy

Contact Info

Product

Resources

About