Diffuse Traumatic Brain Injury Initially Attenuates and Later Expands Activation of the Rat Somatosensory Whisker Circuit Concomitant with Neuroplastic Responses

Brain Res, 2010 · DOI: 10.1016/j.brainres.2010.01.067 · Published: April 6, 2010

Simple Explanation

Traumatic brain injury (TBI) can lead to long-term neurological problems affecting various functions. This study focuses on how TBI affects brain circuits and their ability to reorganize after the initial injury, specifically looking at the whisker-barrel circuit in rats. The study found that after a diffuse brain injury, the whisker somatosensory regions initially showed reduced activation in response to whisker stimulation. However, over time, these regions, along with others like the hippocampus and striatum, showed increased activation, even exceeding normal levels. These changes in activation patterns are linked to neuroplastic responses, where the brain attempts to repair itself by rewiring circuits. However, this rewiring can sometimes lead to maladaptive circuits that contribute to behavioral problems after TBI.

Study Duration

42 Days

Participants

27 adult male Sprague–Dawley rats

Evidence Level

Not specified

Key Findings

1
Whisker somatosensory regions of the cortex and thalamus maintained cellular composition as visualized by Nissl stain.
2
Within the first week post-injury, quantitatively less cFos activation was elicited by whisker stimulation.
3
Over six weeks post-injury, cFos activation after whisker stimulation showed a significant linear correlation with time in the cortex (r2=0.545; p = 0.015), non-significant correlation in the thalamus (r2=0.326) and U-shaped correlation in the denate gyrus (r2=0.831), all eventually exceeding sham levels.

Research Summary

This study investigates how diffuse traumatic brain injury (TBI) affects the activation and reorganization of the whisker-barrel circuit in rats. The researchers hypothesized that the extent of functional activation in brain-injured circuits is a result of initial disruption followed by reorganization. The study found that in the initial week after injury, whisker stimulation resulted in reduced cFos activation in the somatosensory regions. However, over the following six weeks, cFos activation increased in the cortex, thalamus, and dentate gyrus, eventually surpassing sham levels. The researchers suggest that the sprouting of diffuse-injured circuits into diffuse-injured tissue can create maladaptive circuits, leading to behavioral morbidity. They propose that therapeutic interventions to promote adaptive circuit restructuring could help mitigate post-traumatic morbidity.

Practical Implications

Therapeutic interventions

Promoting adaptive circuit restructuring may mitigate post-traumatic morbidity.

Understanding TBI

This study provides a model to explore the causes of persistent morbidity experienced by survivors of mild to moderate TBI.

Maladaptive plasticity

Cellular signaling in the injured brain likely favors axonal growth and survival, with the adverse outcome of maladaptive plasticity.

Study Limitations

1
High background levels of these ubiquitous proteins were not appreciably altered in the diffuse-injured brain (Supplementary Figure 1), affirming immunohistochemistry approaches as insensitive to detect coordinated regenerative responses.
2
In the chronic, diffuse-injured brain distinguishing regenerated circuits from uninjured, intact circuits remains inconclusive.
3
Neuronal atrophy could contribute to the early reductions in cFos activation, whereas the delayed increases in activation are unlikely to be associated with hypertrophy.

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