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10 results on '"Kwok, J C F"'

1. The Chemorepulsive Protein Semaphorin 3A and Perineuronal Net-Mediated Plasticity

Author

de Winter, F, Kwok, J C F, Fawcett, J W, Vo, T T, Carulli, D, Verhaagen, J, de Winter, F, Kwok, J C F, Fawcett, J W, Vo, T T, Carulli, D, and Verhaagen, J

Abstract

During postnatal development, closure of critical periods coincides with the appearance of extracellular matrix structures, called perineuronal nets (PNN), around various neuronal populations throughout the brain. The absence or presence of PNN strongly correlates with neuronal plasticity. It is not clear how PNN regulate plasticity. The repulsive axon guidance proteins Semaphorin (Sema) 3A and Sema3B are also prominently expressed in the postnatal and adult brain. In the neocortex, Sema3A accumulates in the PNN that form around parvalbumin positive inhibitory interneurons during the closure of critical periods. Sema3A interacts with high-affinity with chondroitin sulfate E, a component of PNN. The localization of Sema3A in PNN and its inhibitory effects on developing neurites are intriguing features and may clarify how PNN mediate structural neural plasticity. In the cerebellum, enhanced neuronal plasticity as a result of an enriched environment correlates with reduced Sema3A expression in PNN. Here, we first review the distribution of Sema3A and Sema3B expression in the rat brain and the biochemical interaction of Sema3A with PNN. Subsequently, we review what is known so far about functional correlates of changes in Sema3A expression in PNN. Finally, we propose a model of how Semaphorins in the PNN may influence local connectivity.

Published
2016

6. Developing experimental models of non-traumatic spinal cord injury

Author

Timms, Katherine Victoria, Hall, R. M., Kwok, J. C. F., Tipper, J. L. T., and Ichiyama, R. M.

Subjects
616.8
Abstract

Over 50% of non-traumatic spinal cord injuries (NTSCI) are caused by mechanical compression either due to osteophytes in degenerative disease, or tumours (New et al., 2014). The pathophysiology of NTSCI is poorly understood, with no distinct injury cascade (Karadimas et al., 2013). The aim of this project was to evaluate cellular responses to mechanical insults in the context of NTSCI. In-vitro, a model was developed to apply high and low velocity compression to astrocyte-seeded collagen hydrogels. Outcomes included hydrogel contraction, GFAP expression, cellular shape, and cytokine release. In-vivo a balloon lesion model was modified to induce a non-traumatic ventral lesion, by developing an injection port and inflating over 3 days. Functional deficits and histological outcomes were assessed. In-vitro, 100 mm.s-1 compression elicited an astrogliotic and inflammatory response from day 11, indicative of TSCI. This comprised a significant increase in GFAP area per cell, astrocyte ramification, and IL-6 expression. Conversely, at < 100 mm.s-1, no differences were observed. The findings of this study suggest slow compression of astrocytes alone does not induce NTSCI. In-vivo, surgery was undertaken on 10 animals (including 3 shams). In injury groups, functional deficits were observed , which increased with each inflation. Animals were grouped into mild and severe based on their motor function (severe animals exhibited paraplegia). Minimum motor function correlated with minimum cross-sectional area, and greater parenchyma disruption. In the severe group only, there was a trend of mild astrogliosis, demyelination and vasculature narrowing at the epicentre. This corresponds with the wider literature, where demyelination and disruption to the vasculature are hypothesised to be involved in NTSCI pathology. Overall, in-vitro and in-vivo models of NTSCI have been successfully developed. Physiological changes were observed in both models, with differences to TSCI. Further investigations can be undertaken to understand the pathology of NTSCI.

Published
2020

7. Chondroitin 6-sulphate is required for neuroplasticity and memory in ageing

Author

James W. Fawcett, Chin Lik Tan, Yuko Naito-Matsui, Timothy M. Bussey, Tommaso Pizzorusso, Sam Hilton, Bart Nieuwenhuis, Lisa M. Saksida, Sujeong Yang, Jessica C. F. Kwok, Joost Verhaagen, Sylvain Gigout, Simona Foscarin, Angelo Molinaro, Hiroshi Kitagawa, Netherlands Institute for Neuroscience (NIN), Molinaro, Angelo [0000-0002-8539-4429], Nieuwenhuis, Bart [0000-0002-2065-2271], Kwok, Jessica CF [0000-0002-9798-9083], Fawcett, James [0000-0002-7990-4568], Apollo - University of Cambridge Repository, Fawcett, James W [0000-0002-7990-4568], Yang, S., Gigout, S., Molinaro, A., Naito-Matsui, Y., Hilton, S., Foscarin, S., Nieuwenhuis, B., Tan, C. L., Verhaagen, J., Pizzorusso, T., Saksida, L. M., Bussey, T. M., Kitagawa, H., Kwok, J. C. F., and Fawcett, J. W.

Subjects
0301 basic medicine, Aging, Transgene, Biology, Inhibitory postsynaptic potential, Biochemistry, Settore BIO/09 - Fisiologia, Article, 03 medical and health sciences, Cellular and Molecular Neuroscience, chemistry.chemical_compound, Mice, 0302 clinical medicine, Neuroplasticity, Memory impairment, Chondroitin, Animals, Molecular Biology, Neuronal Plasticity, Perineuronal net, Chondroitin Sulfates, Brain, Long-term potentiation, Extracellular Matrix, Psychiatry and Mental health, 030104 developmental biology, chemistry, Ageing, Neuroscience, 030217 neurology & neurosurgery
Abstract

Funder: Alzheimers research UK, Perineuronal nets (PNNs) are chondroitin sulphate proteoglycan-containing structures on the neuronal surface that have been implicated in the control of neuroplasticity and memory. Age-related reduction of chondroitin 6-sulphates (C6S) leads to PNNs becoming more inhibitory. Here, we investigated whether manipulation of the chondroitin sulphate (CS) composition of the PNNs could restore neuroplasticity and alleviate memory deficits in aged mice. We first confirmed that aged mice (20-months) showed memory and plasticity deficits. They were able to retain or regain their cognitive ability when CSs were digested or PNNs were attenuated. We then explored the role of C6S in memory and neuroplasticity. Transgenic deletion of chondroitin 6-sulfotransferase (chst3) led to a reduction of permissive C6S, simulating aged brains. These animals showed very early memory loss at 11 weeks old. Importantly, restoring C6S levels in aged animals rescued the memory deficits and restored cortical long-term potentiation, suggesting a strategy to improve age-related memory impairment.

Published
2021

8. MiR-29 coordinates age-dependent plasticity brakes in the adult visual cortex

Author

Eva Terzibasi Tozzini, Tommaso Pizzorusso, Pierre Baldi, Sara Bagnoli, Joanna Kirkpartick, Giulia Sagona, Siwei Chen, Muntaha Samad, Alessandro Cellerino, Erika Kelmer Sacramento, Elena Putignano, Paola Tognini, Jessica C. F. Kwok, Leonardo Lupori, Raffaele Mazziotti, Debora Napoli, Napoli, D., Lupori, L., Mazziotti, R., Sagona, G., Bagnoli, S., Samad, M., Sacramento, E. K., Kirkpartick, J., Putignano, E., Chen, S., Terzibasi Tozzini, E., Tognini, P., Baldi, P., Kwok, J. C. F., Cellerino, A., and Pizzorusso, T.

Subjects
Proteomics, Period (gene), Regulator, Biology, Plasticity, Inbred C57BL, Biochemistry, Settore BIO/09 - Fisiologia, Ocular dominance, 03 medical and health sciences, chemistry.chemical_compound, Mice, ocular dominance plasticity, 0302 clinical medicine, Ocular, microRNA, Genetics, medicine, Animals, 2.1 Biological and endogenous factors, Antagomir, Aetiology, Molecular Biology, Eye Disease and Disorders of Vision, Dominance, 030304 developmental biology, Visual Cortex, 0303 health sciences, Neuronal Plasticity, DNA methylation, Perineuronal net, perineuronal net, Articles, Dominance, Ocular, Mice, Inbred C57BL, MicroRNAs, Visual cortex, medicine.anatomical_structure, chemistry, Biochemistry and Cell Biology, Neuroscience, 030217 neurology & neurosurgery, Biotechnology, Developmental Biology
Abstract

Visual cortical circuits show profound plasticity during early life and are later stabilized by molecular "brakes" limiting excessive rewiring beyond a critical period. The mechanisms coordinating the expression of these factors during the transition from development to adulthood remain unknown. We found that miR-29a expression in the visual cortex dramatically increases with age, but it is not experience-dependent. Precocious high levels of miR-29a blocked ocular dominance plasticity and caused an early appearance of perineuronal nets. Conversely, inhibition of miR-29a in adult mice using LNA antagomirs activated ocular dominance plasticity, reduced perineuronal nets, and restored their juvenile chemical composition. Activated adult plasticity had the typical functional and proteomic signature of critical period plasticity. Transcriptomic and proteomic studies indicated that miR-29a manipulation regulates the expression of plasticity brakes in specific cortical circuits. These data indicate that miR-29a is a regulator of the plasticity brakes promoting age-dependent stabilization of visual cortical connections.

Published
2020

9. Adaptation of tape removal test for measurement of sensitivity in perineal area of rat.

Author

Neumannova K, Machova-Urdzikova L, Kwok JCF, Fawcett JW, and Jendelova P

Subjects
Animals, Behavior, Animal, Female, Genitalia injuries, Male, Physical Stimulation, Rats, Rats, Inbred Lew, Rats, Long-Evans, Rats, Sprague-Dawley, Rats, Wistar, Sensation Disorders etiology, Sensation Disorders psychology, Skin injuries, Species Specificity, Spinal Cord Injuries psychology, Adaptation, Psychological, Perineum injuries, Perineum physiology
Abstract

Regeneration after spinal cord injury is a goal of many studies. Although the most obvious target is to recover motor function, restoration of sensation can also improve the quality of life after spinal cord injury. For many patients, recovery of sensation in the perineal and genital area is a high priority. Currently there is no experimental test in rodents for measuring changes in sensation in the perineal and genital area after spinal cord injury. The aim of our study was to develop a behavioural test for measuring the sensitivity of the perineal and genital area in rats. We have modified the tape removal test used routinely to test sensorimotor deficits after stroke and spinal cord injury to test the perineal area with several variations. A small piece of tape (approximately 1 cm 2 ) was attached to the perineal area. Time to first contact and to the removal of the tape was measured. Each rat was trained for 5 consecutive days and then tested weekly. We compared different rat strains (Wistar, Sprague-Dawley, Long-Evans and Lewis), both genders, shaving and non-shaving and different types of tape. We found that the test was suitable for all tested strains, however, Lewis rats achieved the lowest contact times, but this difference was significant only for the first few days of learning the task. There were no significant differences between gender and different types of tape or shaving. After training the animals underwent dorsal column lesion at T10 and were tested at day 3, 8, 14 and 21. The test detected a sensory deficit, the average time across all animals to sense the stimulus increased from 1'32 up to 3'20. There was a strong relationship between lesion size and tape detection time, and only lesions that extended laterally to the dorsal root entry zone produced significant sensory deficits. Other standard behavioural tests (BBB, von Frey, ladder and Plantar test) were performed in the same animals. There was a correlation between lesion size and deficit for the ladder and BBB tests, but not for the von Frey and Plantar tests. We conclude that the tape removal test is suitable for testing perineal sensation in rats, can be used in different strains and is appropriate for monitoring changes in sensation after spinal cord injury., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Published
2020
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10. Chondroitin sulfate: a key molecule in the brain matrix.

Author

Kwok JC, Warren P, and Fawcett JW

Subjects
Animals, Brain physiology, Brain Injuries metabolism, Brain Injuries physiopathology, Chondroitin Sulfates biosynthesis, Chondroitin Sulfates chemistry, Gene Expression Regulation, Humans, Neuronal Plasticity, Spinal Cord Injuries metabolism, Spinal Cord Injuries physiopathology, Brain metabolism, Chondroitin Sulfates metabolism
Abstract

Chondroitin sulfate is a glycosaminoglycan composed of N-acetylgalactosamine and glucuronic acid. It attaches to a core protein to form chondroitin sulfate proteoglycan (CSPG). Being a major component of the brain extracellular matrix, CSPGs are involved in neural development, axon pathfinding and guidance, plasticity and also regeneration after injury in the nervous system. In this review, we shall discuss the structure, the biosynthetic pathway, its functions in the nervous system and how we can improve regeneration in the nervous system by modulating its structure and binding properties., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Published
2012
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