Comparison of rat sensory behavioral tasks to detect somatosensory morbidity after diffuse brain-injury

Learoyd, Annastazia E.; Lifshitz, Jonathan

doi:10.1016/j.bbr.2011.09.016

Cited by 36 publications

(41 citation statements)

References 40 publications

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“…35,36,[96][97][98] The P4 amelioration of hyper-sensitive to whisker stimulation may translate to reduced sensory sensitivity in people with severe TBI or reflect changes in anxiety, a factor in the whisker nuisance task. 44,95 This is consistent with reports of lower anxiety outcomes in TBI subjects treated with progesterone. 99 Overall, our results mirror recent results showing no beneficial outcome of P4 treatment in patients with moderate-to-severe TBI, 31 in contrast to the clinical trials reporting positive effects of using P4 as a therapeutic option 26,27 which were conducted using patients with mild to moderate TBI.…”

supporting

confidence: 88%

“…Changes in whisker based processing following injury are associated with thalamic neural damage and atrophy. 44,95 Sensory deficiencies and hyper-sensitivity have been reported in TBI patients. 35,36,[96][97][98] The P4 amelioration of hyper-sensitive to whisker stimulation may translate to reduced sensory sensitivity in people with severe TBI or reflect changes in anxiety, a factor in the whisker nuisance task.…”

mentioning

confidence: 99%

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Progesterone Exacerbates Short-Term Effects of Traumatic Brain Injury on Supragranular Responses in Sensory Cortex and Over-Excites Infragranular Responses in the Long Term

Allitt

Johnstone

Richards

et al. 2016

Journal of Neurotrauma

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Progesterone (P4) has been suggested as a neuroprotective agent for traumatic brain injury (TBI) because it ameliorates many post-TBI sequelae. We examined the effects of P4 treatment on the short-term (4 days post-TBI) and long-term (8 weeks post-TBI) aftermath on neuronal processing in the rodent sensory cortex of impact acceleration-induced diffuse TBI. We have previously reported that in sensory cortex, diffuse TBI induces a short-term hypoexcitation that is greatest in the supragranular layers and decreases with depth, but a long-term hyperexcitation that is exclusive to the supragranular layers. Now, adult male TBI-treated rats administered P4 showed, in the short term, even greater suppression in neural responses in supragranular layers but a reversal of the TBI-induced suppression in granular and infragranular layers. In long-term TBI there were only inconsistent effects of P4 on the TBI-induced hyperexcitation in supragranular responses but infragranular responses, which were not affected by TBI alone, were elevated by P4 treatment. Intriguingly, the effects in the injured brain were almost identical to P4 effects in the normal brain, as seen in sham control animals treated with P4: in the short term, P4 effects in the normal brain were identical to those exercised in the injured brain and in the long term, P4 effects in the normal brain were rather similar to what was seen in the TBI brain. Overall, these results provide no support for any protective effects of P4 treatment on neuronal encoding in diffuse TBI, and this was reflected in sensorimotor and other behavior tasks also tested here. Additionally, the effects suggest that mechanisms used for P4 effects in the normal brain are also intact in the injured brain.

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confidence: 88%

mentioning

confidence: 99%

Progesterone Exacerbates Short-Term Effects of Traumatic Brain Injury on Supragranular Responses in Sensory Cortex and Over-Excites Infragranular Responses in the Long Term

Allitt

Johnstone

Richards

et al. 2016

Journal of Neurotrauma

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“…The pathology in these regions is hypothesized to arise from the thickened temporal ridges that overlie the S1BF (Lifshitz et al 2011). The neuronal changes were concomitant with late onset, persistent, abnormal behavioral responses to whisker stimulation in brain-injured animals (McNamara et al 2010;Learoyd and Lifshitz 2012;Thomas et al 2012). Similar pathology, as measured by neuronal morphology, is evident in the somatosensory cortex of the diffuse-injured mouse (Greer et al 2011).…”

Section: Study Aimmentioning

confidence: 99%

“…In impact-acceleration models, movement of the neck could account for a mechanical origin of the pathology, whereas fixed head models may result in brainstem pathology as a result of delayed degenerative processes. It is important to note that post-injury morbidities, such as sensory sensitivity, tend to manifest several weeks after experimental diffuse brain injury is induced (McNamara et al 2010;Learoyd and Lifshitz 2012;Thomas et al 2012), but the extent of pathology in critical brainstem nuclei (PrV and VIIN) is unknown. Thus, we were prompted to investigate the time course of neuropathology and glial pathology in these brainstem regions.…”

Section: Study Aimmentioning

confidence: 99%

Neuropathology in sensory, but not motor, brainstem nuclei of the rat whisker circuit after diffuse brain injury

Miremami

Talauliker

Harrison

et al. 2014

Somatosensory & Motor Research

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Neurological dysfunction after traumatic brain injury (TBI) is associated with pathology in cortical, subcortical, and brainstem nuclei. Our laboratory has reported neuropathology and microglial activation in the somatosensory barrel cortex (S1BF) and ventral posterior medial thalamus (VPM) after diffuse TBI in the rat, which correlated with post-injury whisker sensory sensitivity. The present study extends our previous work by evaluating pathology in whisking-associated sensory and motor brainstem nuclei. Brains from adult, male rats were recovered over 1 month after midline fluid percussion or sham injury. The principal trigeminal nucleus (PrV, sensory nucleus) and facial nucleus (VIIN, motor nucleus) were examined for neuropathology (silver histochemistry) and microglial activation (Iba1). Significant neuropathology in PrV was evident at 2 and 7 days post-injury compared to sham. Iba1-labeled microglia showed swollen somata and thickened processes over 1 month post-injury. In contrast, the VIIN showed non-significant neuropathology and reduced labeling of activated Iba1 microglia over 1 month post-injury. Together with our previous data, neuropathology and neuroinflammation in the whisker somatosensory pathway may contribute to post-injury sensory sensitivity more than the motor pathway. Whether these findings are direct results of the mechanical injury or consequences of progressive degeneration remains to be determined.

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“…Sensory sensitivity has been assessed with a whisker nuisance task, in which whisker stimulation elicts aggravated behavioral responses after mild FPI. 62,63 Balance/coordination has been studied with beam balance and walking tasks, and the rotarod task.…”

Section: Limitations Of Current Mild Injury Modelsmentioning

confidence: 99%

Mild Traumatic Brain Injury in Translation

Levin

Robertson

2013

Journal of Neurotrauma

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This Introduction to a Special Issue on Mild Traumatic Brain Injury (mTBI) highlights the methodological challenges in outcome studies and clinical trials involving patients who sustain mTBI. Recent advances in brain imaging and portable, computerized cognitive tasks have contributed to protocols that are sensitive to the effects of mTBI and efficient in time for completion. Investigation of civilian mTBI has been extended to single and repeated injuries in athletes and blastrelated mTBI in service members and veterans. Despite differences in mechanism of injury, there is evidence for similar effects of acceleration-deceleration and blast mechanisms of mTBI on cognition. Investigation of repetitive mTBI suggests that the effects may be cumulative and that repeated mTBI and repeated subconcussive head trauma may lead to neurodegenerative conditions. Although animal models of mTBI using cortical impact and fluid percussion injury in rodents have been able to reproduce some of the cognitive deficits frequently exhibited by patients after mTBI, modeling post-concussion symptoms is difficult. Recent use of closed head and blast injury animal models may more closely approximate clinical mTBI. Translation of interventions that are developed in animal models to patients with mTBI is a priority for the research agenda. This Special Issue on mTBI integrates basic neuroscience studies using animal models with studies of human mTBI, including the cognitive sequelae, persisting symptoms, brain imaging, and host factors that facilitate recovery.

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Comparison of rat sensory behavioral tasks to detect somatosensory morbidity after diffuse brain-injury

Cited by 36 publications

References 40 publications

Progesterone Exacerbates Short-Term Effects of Traumatic Brain Injury on Supragranular Responses in Sensory Cortex and Over-Excites Infragranular Responses in the Long Term

Progesterone Exacerbates Short-Term Effects of Traumatic Brain Injury on Supragranular Responses in Sensory Cortex and Over-Excites Infragranular Responses in the Long Term

Neuropathology in sensory, but not motor, brainstem nuclei of the rat whisker circuit after diffuse brain injury

Mild Traumatic Brain Injury in Translation

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