Neural Plasticity and Neurorehabilitation Following Traumatic Brain Injury

2010 ◽  
Author(s):  
Dorothy Kozlowski
2020 ◽  
Author(s):  
Samantha N. Schumm ◽  
David Gabrieli ◽  
David F. Meaney

AbstractPatients who suffer from traumatic brain injury (TBI) often complain of learning and memory problems. Their symptoms are principally mediated by the hippocampus and the ability to adapt to stimulus, also known as neural plasticity. Therefore, one plausible injury mechanism is plasticity impairment, which currently lacks comprehensive investigation across TBI research. For these studies, we used a computational network model of the hippocampus that includes the dentate gyrus, CA3, and CA1 with neuron-scale resolution. We simulated mild injury through weakened spike-timing-dependent plasticity (STDP), which modulates synaptic weights according to causal spike timing. In preliminary work, we found functional deficits consisting of decreased firing rate and broadband power in areas CA3 and CA1 after STDP impairment. To address structural changes with these studies, we applied modularity analysis to evaluate how STDP impairment modifies community structure in the hippocampal network. We also studied the emergent function of network-based learning and found that impaired networks could acquire conditioned responses after training, but the magnitude of the response was significantly lower. Furthermore, we examined pattern separation, a prerequisite of learning, by entraining two overlapping patterns. Contrary to our initial hypothesis, impaired networks did not exhibit deficits in pattern separation with either population- or rate-based coding. Collectively, these results demonstrate how a mechanism of injury that operates at the synapse regulates circuit function.Author summaryTraumatic brain injury causes diverse symptoms, and memory problems are common among patients. These deficits are associated with the hippocampus, a brain region involved in learning and memory. Neural plasticity supports learning and memory by enabling the circuit to adapt to external stimulus. After brain injury, plasticity can be impaired, perhaps contributing to memory deficits. Yet, this mechanism of injury remains poorly understood. We implemented plasticity impairment and learning in a network model of the hippocampus that is unique because it has a high degree of biological detail in its structure and dynamics compared to other similar computational models. First, we examined the relationship between neurons in the network and characterized how the structure changed with injury. Then we trained the network with two input patterns to test the function of pattern separation, which is the ability to distinguish similar contexts and underpins general learning. We found that the strength of the encoded response decreased after impairment, but the circuit could still distinguish the two input patterns. This work provides insight into which specific aspects of memory become dysfunctional after injury.


2016 ◽  
Vol 3 (4) ◽  
Author(s):  
Linda Marschner ◽  
Tariq Ahmed ◽  
An Schreurs ◽  
Benoit Lechat ◽  
Fred Van Leuven ◽  
...  

2021 ◽  
Vol 2 (1) ◽  
pp. 200-213
Author(s):  
Ann N. Hoffman ◽  
Sonya Watson ◽  
Michael S. Fanselow ◽  
David A. Hovda ◽  
Christopher Giza

1997 ◽  
Vol 21 (5) ◽  
pp. 171
Author(s):  
A Boggs ◽  
P Kraemer ◽  
R Brown ◽  
D Leider ◽  
K B Seroogy ◽  
...  

2019 ◽  
Vol 14 (5) ◽  
pp. 1638-1650 ◽  
Author(s):  
Shun-Chin Jim Wu ◽  
Lisanne M. Jenkins ◽  
Alexandra C. Apple ◽  
Julie Petersen ◽  
Furen Xiao ◽  
...  

2007 ◽  
pp. 359-368
Author(s):  
M Lippert-Grüner ◽  
M Maegele ◽  
J Pokorný ◽  
DN Angelov ◽  
O Švestková ◽  
...  

This study used an experimental early rehabilitation model combining an enriched environment, multisensory (visual, acoustic and olfactory) stimulation and motor training after traumatic brain injury (via fluid-percussion model) to simulate early multisensory rehabilitation. This therapy will be used by brain injured patients to improve neural plasticity and to restore brain integration functions. Motor dysfunction was evaluated using a composite neuroscore test. Direct structural effects of traumatic brain injury were examined using Fluoro-Jade staining, which allows identification of degenerating neural cell bodies and processes. Animals in the rehabilitation model group performed significantly better when tested for neuromotor function than the animals in standard housing in the 7-day and 15-day interval after injury (7d: p=0.005; 15d: p<0.05). Statistical analysis revealed significantly lower numbers of Fluoro-Jade positive cells (degenerating neurons) in the rehabilitation model group (n=5: mean 13.4) compared to the standard housing group (n=6: mean 123.8) (p<0.005). It appears that the housing of animals in the rehabilitation model led to a clear functional increase in neuromotor functions and to reduced neural loss compared with the animal group in standard housing.


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