scholarly journals Experience-dependent plasticity mechanisms for neural rehabilitation in somatosensory cortex

2008 ◽  
Vol 364 (1515) ◽  
pp. 369-381 ◽  
Author(s):  
Kevin Fox
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Somatosensory Cortex ◽  
Barrel Cortex ◽  
Cortical Plasticity ◽  
Sensory Experience ◽  
Functional Rehabilitation ◽  
Central Nervous System Damage ◽  
Dependent Plasticity

Functional rehabilitation of the cortex following peripheral or central nervous system damage is likely to be improved by a combination of behavioural training and natural or therapeutically enhanced synaptic plasticity mechanisms. Experience-dependent plasticity studies in the somatosensory cortex have begun to reveal those synaptic plasticity mechanisms that are driven by sensory experience and might therefore be active during behavioural training. In this review the anatomical pathways, synaptic plasticity mechanisms and structural plasticity substrates involved in cortical plasticity are explored, focusing on work in the somatosensory cortex and the barrel cortex in particular.

scholarly journals Is there a thalamic component to experience–dependent cortical plasticity?

2002 ◽  
Vol 357 (1428) ◽  
pp. 1709-1715 ◽  
Author(s):  
Kevin Fox ◽  
Helen Wallace ◽  
Stanislaw Glazewski
Keyword(s):  
Nervous System ◽  
Somatosensory Cortex ◽  
Peripheral Nervous System ◽  
Lateral Inhibition ◽  
Cortical Plasticity ◽  
Sensory Deprivation ◽  
Receptive Fields ◽  
Somatosensory System ◽  
Cortical Cells ◽  
Dependent Plasticity

Sensory deprivation and injury to the peripheral nervous system both induce plasticity in the somatosensory system of adult animals, but in different places. While injury induces plasticity at several locations within the ascending somatosensory pathways, sensory deprivation appears only to affect the somatosensory cortex. Experiments have been performed to detect experience–dependent plasticity in thalamic receptive fields, thalamic domain sizes and convergence of thalamic receptive fields onto cortical cells. So far, plasticity has not been detected with sensory deprivation paradigms that cause substantial cortical plasticity. Part of the reason for the lack of thalamic plasticity may lie in the synaptic properties of afferent systems to the thalamus. A second factor may lie in the differences in the organization of cortical and thalamic circuits. Many deprivation paradigms induce plasticity by decreasing phasic lateral inhibition. Since lateral inhibition appears to be far weaker in the thalamus than the cortex, sensory deprivation may not cause large enough imbalances in thalamic activity to induce plasticity in the thalamus.

scholarly journals The Function of Selenium in Central Nervous System: Lessons from MsrB1 Knockout Mouse Models

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1372
Author(s):  
Tengrui Shi ◽  
Jianxi Song ◽  
Guanying You ◽  
Yujie Yang ◽  
Qiong Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Mouse Models ◽  
Knockout Mouse ◽  
Methionine Sulfoxide ◽  
Methionine Sulfoxide Reductase ◽  
Knockout Mouse Model ◽  
The Central Nervous System

MsrB1 used to be named selenoprotein R, for it was first identified as a selenocysteine containing protein by searching for the selenocysteine insert sequence (SECIS) in the human genome. Later, it was found that MsrB1 is homologous to PilB in Neisseria gonorrhoeae, which is a methionine sulfoxide reductase (Msr), specifically reducing L-methionine sulfoxide (L-Met-O) in proteins. In humans and mice, four members constitute the Msr family, which are MsrA, MsrB1, MsrB2, and MsrB3. MsrA can reduce free or protein-containing L-Met-O (S), whereas MsrBs can only function on the L-Met-O (R) epimer in proteins. Though there are isomerases existent that could transfer L-Met-O (S) to L-Met-O (R) and vice-versa, the loss of Msr individually results in different phenotypes in mice models. These observations indicate that the function of one Msr cannot be totally complemented by another. Among the mammalian Msrs, MsrB1 is the only selenocysteine-containing protein, and we recently found that loss of MsrB1 perturbs the synaptic plasticity in mice, along with the astrogliosis in their brains. In this review, we summarized the effects resulting from Msr deficiency and the bioactivity of selenium in the central nervous system, especially those that we learned from the MsrB1 knockout mouse model. We hope it will be helpful in better understanding how the trace element selenium participates in the reduction of L-Met-O and becomes involved in neurobiology.

Brain organoids: a promising model to assess oxidative stress‐induced Central Nervous System damage

2021 ◽  
Author(s):  
Foluwasomi A. Oyefeso ◽  
Alysson R. Muotri ◽  
Christopher G. Wilson ◽  
Michael J. Pecaut
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Damage

scholarly journals Troublesome Heterotopic Ossification after Central Nervous System Damage: A Survey of 570 Surgeries

PLoS ONE ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. e16632 ◽  
Author(s):  
François Genêt ◽  
Claire Jourdan ◽  
Alexis Schnitzler ◽  
Christine Lautridou ◽  
Didier Guillemot ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Heterotopic Ossification ◽  
Central Nervous System Damage

scholarly journals Design and Implementation ofReal-time Electrical Stimulation Artifact Suppression based on STM32

2021 ◽  
Vol 12 (5) ◽  
pp. 424-427
Author(s):  
Sangsoo Park, Hojun Yeom
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Electrical Stimulation ◽  
Embedded System ◽  
Muscle Contraction ◽  
Real Time ◽  
High Performance ◽  
Floating Point ◽  
Time Signal ◽  
Central Nervous System Damage

A biosignal is used as a control signal for electrical stimulation to restore weakened muscle function due to damage to the central nervous system. In patients with central nervous system damage, sufficient muscle contraction does not occur spontaneously. In this case, applying electrical stimulation can cause normal muscle contraction. However, it is necessary to remove the electrical stimulation artifact caused by the electrical stimulation. This paper describes a system design that removes electrical stimulation artifact in real time using a Cortex-M4-based STM32F processor. The STM32F is a very advantageous MCU for such DSPs, especially because it has a built-in floating point operator. Using STM32F's various high-performance peripherals (12-bit parallel ADC and 12-bit DAC, UART, Timer), an optimized embedded system was implemented.In this paper, the simulated and real-time results were compared and evaluated with the designed fir filter. In addition, the performance of the filter was evaluated through frequency analysis. As a result, it was verified that a high-performance 32-bit STM32F with floating point calculator and various peripherals is suitable for real-time signal processing

scholarly journals Mycobacterium of tuberculosis with defective cell wall, determined in the brain of the biological model with spongional changes

2019 ◽  
Vol 23 (1) ◽  
pp. 12-19
Author(s):  
O.P. Lysenko ◽  
V.V. Vlasenko ◽  
H.K. Palii ◽  
I.H. Vlasenko ◽  
O.A. Nazarchuk
Keyword(s):  
Central Nervous System ◽  
Cell Wall ◽  
Nervous System ◽  
Mycobacterium Tuberculosis ◽  
Brain Damage ◽  
Molecular Genetic Study ◽  
Central Nervous System Damage ◽  
Infectious Dose ◽  
Microbiological Methods ◽  
The Brain

Mycobacterium tuberculosis is endowed with resistance to adverse factors and rapidly forms drug resistance. The aim is to study of the connection of tuberculosis infection and the development of brain damage with signs of spongymorphic changes. There were investigated canned 10% formalin fragments of the brain of 2 goats with signs of central nervous system damage by histological, microbiological methods. For microbiological examination, 3–5 years brain samples after were sowed on the MycСel DW nutrient medium with a growth stimulator. The molecular genetic study was performed using a polymerase chain reaction on a Molecular Imager GelDoc TM XR + (BioRad) device. The polypeptide profile was studied electrophoretically. In the goats, who died with symptoms of central nervous system damage, spongiform changes were detected in the brain. In the brain samples, DNA and mycobacterium tuberculosis with a defective cell wall have been detected, accumulation of mycobacterial antigens has been observed in the cells of the brain and in the intercellular space. Despite the fact that brain samples were in 10% formalin for 1 month, 3 years and 5 years, in all cases mycobacterium tuberculosis with a defective cell wall was isolated. Their viability was comparable to the infectiousness of prions. The isolation of mycobacterium tuberculosis with a defective cell wall from the brain did not differ in morphology and polypeptide composition from isolates from tuberculin, FLK-BLV, lymph nodes of cows, patients with tuberculosis. This indicates a high probability that mycobacterial infection, depending on the infectious dose, the characteristics of the strain and host genome, as well as the state of the immune system, can cause oncogenic action, cause active tuberculosis, brain damage, and the cardiovascular system.

scholarly journals The central nervous system is a target of acute graft versus host disease in mice

Blood ◽  
2013 ◽  
Vol 121 (10) ◽  
pp. 1906-1910 ◽  
Author(s):  
Steffen Hartrampf ◽  
Jarrod A. Dudakov ◽  
Linda K. Johnson ◽  
Odette M. Smith ◽  
Jennifer Tsai ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Damage ◽  
Graft Versus Host ◽  
Alloreactive T Cells ◽  
Key Points ◽  
The Central Nervous System ◽  
Anxiety Behavior ◽  
Direct Target ◽  
Acute Graft

Key Points The central nervous system can be a direct target of alloreactive T cells during GVHD. Central nervous system damage in mouse models of GVHD lead to deficits in learning and increased anxiety behavior.

LONGITUDINAL STUDY OF THE INCIDENCE OF CENTRAL NERVOUS SYSTEM DAMAGE FOLLOWING ERYTHROBLASTOSIS FETALIS

PEDIATRICS ◽  
1954 ◽  
Vol 14 (4) ◽  
pp. 346-350
Author(s):  
MARGARET H. JONES ◽  
RUSSELL SANDS ◽  
CAROL B. HYMAN ◽  
PHILLIP STURGEON ◽  
FREMONT P. KOCH
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Longitudinal Study ◽  
Central Nervous System Involvement ◽  
Newborn Period ◽  
Central Nervous System Damage ◽  
System Involvement ◽  
Childrens Hospital ◽  
Infancy And Childhood

One hundred unselected cases of erythroblastosis fetalis treated at Childrens Hospital in the newborn period have been followed from six months to five years in an effort to evaluate the relation of central nervous system signs in the newborn period to neuromuscular handicap and overall development later. Of those showing no central nervous system signs in the newborn period 4% showed definite abnormality later. Of those showing equivocal signs in the newborn period 33% showed definite abnormality later. Of those having definite signs early, 100% continued to show abnormality in infancy and childhood. There was no relation of the severity of the signs in the newborn period to the severity of the later handicap. It is suggested, therefore, that one cannot be certain of the later normality of an infant showing no definite or equivocal central nervous system involvement in the newborn period. Careful following of all erythroblastotic infants until six to eight years of age or longer is advisable.

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