Reduced sensorimotor reactivity following traumatic brain injury in rats

Wiley, Jenny L.; Compton, Amelia D.; Pike, Brian R.; Temple, Meredith D.; McElderry, Jonathan W.; Hamm, Robert J.

doi:10.1016/0006-8993(96)00045-5

Cited by 21 publications

(16 citation statements)

References 23 publications

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“…Furthermore, in vivo studies indicate that evoked potentials and sensorimotor reactivity are also abnormal (DeSalles et al, 1987;Shaw, 1986;Wiley et al, 1996). Consequently, it is not surprising that the cerebral metabolic responsiveness to somatosensory circuit activation via vibrissa stimulation is depressed in the ipsilateral trigeminal medullary complex, contralateral ventrobasal thalamus, and primary somatosensory cortex in rats up to 2 months after LFPI (Dietrich et al, 1994;Passineau et al, 2000).…”

Section: Response To Activation After Traumatic Brain Injurymentioning

confidence: 99%

Metabolic, Neurochemical, and Histologic Responses to Vibrissa Motor Cortex Stimulation after Traumatic Brain Injury

Zanier

Moore

et al. 2003

J Cereb Blood Flow Metab

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Summary: During the prolonged metabolic depression after traumatic brain injury (TBI), neurons are less able to respond metabolically to peripheral stimulation. Because this decreased responsiveness has been attributed to circuit dysfunction, the present study examined the metabolic, neurochemical, and histologic responses to direct cortical stimulation after lateral fluid percussion injury (LFPI). This study addressed three specific hypotheses: that neurons, if activated after LFPI, will increase their utilization of glucose even during a period of posttraumatic metabolic depression; that this secondary activation results in an increase in the production of lactate and a depletion of extracellular glucose; and that because cells are known to be in a state of energy crisis after traumatic brain injury, additional energy demands resulting from activation can result in their death. The results indicate that stimulating to levels eliciting a vibrissa twitch resulted in an increase in the cerebral metabolic rate for glucose (CMR glc ; mol·100 g ) of 34% to 61% in the sham-operated, 1-hour LFPI, and 7-day LFPI groups.However, in the 1-day LFPI group, stimulation induced a 161% increase in CMR glc and a 35% decrease in metabolic activation volume. Extracellular lactate concentrations during stimulation significantly increased from 23% in the sham-injured group to 55% to 63% in the 1-day and 7-day LFPI groups. Extracellular glucose concentrations during stimulation remained unchanged in the sham-injured and 7-day LFPI groups, but decreased 17% in the 1-day LFPI group. The extent of cortical degeneration around the stimulating electrode in the 1-day LFPI group nearly doubled when compared with controls. These results indicate that at 1 day after LFPI, the cortex can respond to stimulation with an increase in anaerobic glycolysis; however, this metabolic response to levels eliciting a vibrissa response via direct cortical stimulation appears to constitute a secondary injury in the TBI brain.

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Section: Response To Activation After Traumatic Brain Injurymentioning

confidence: 99%

Metabolic, Neurochemical, and Histologic Responses to Vibrissa Motor Cortex Stimulation after Traumatic Brain Injury

Zanier

Moore

et al. 2003

J Cereb Blood Flow Metab

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“…Blocking this activity after ischemic lesions prevents axonal sprouting (Carmichael and Chesselet, 2002). In vitro and in vivo studies have shown that electrophysiological responses and cellular excitability post-TBI are impaired (DeSalles et al, 1987;Reeves et al, 2000;Wiley et al, 1996). This impairment in cellular excitability post-TBI may prevent plastic structural changes.…”

Section: Figmentioning

confidence: 99%

Use-Dependent Dendritic Regrowth Is Limited after Unilateral Controlled Cortical Impact to the Forelimb Sensorimotor Cortex

Jones

Liput

Maresh

et al. 2012

Journal of Neurotrauma

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Compensatory neural plasticity occurs in both hemispheres following unilateral cortical damage incurred by seizures, stroke, and focal lesions. Plasticity is thought to play a role in recovery of function, and is important for the utility of rehabilitation strategies. Such effects have not been well described in models of traumatic brain injury (TBI). We examined changes in immunoreactivity for neural structural and plasticity-relevant proteins in the area surrounding a controlled cortical impact (CCI) to the forelimb sensorimotor cortex (FL-SMC), and in the contralateral homotopic cortex over time (3-28 days). CCI resulted in considerable motor deficits in the forelimb contralateral to injury, and increased reliance on the ipsilateral forelimb. The density of dendritic processes, visualized with immunostaining for microtubule-associated protein-2 (MAP-2), were bilaterally decreased at all time points. Synaptophysin (SYN) immunoreactivity increased transiently in the injured hemisphere, but this reflected an atypical labeling pattern, and it was unchanged in the contralateral hemisphere compared to uninjured controls. The lack of compensatory neuronal structural plasticity in the contralateral homotopic cortex, despite behavioral asymmetries, is in contrast to previous findings in stroke models. In the cortex surrounding the injury (but not the contralateral cortex), decreases in dendrites were accompanied by neurodegeneration, as indicated by Fluoro-Jade B (FJB) staining, and increased expression of the growth-inhibitory protein Nogo-A. These studies indicate that, following unilateral CCI, the cortex undergoes neuronal structural degradation in both hemispheres out to 28 days post-injury, which may be indicative of compromised compensatory plasticity. This is likely to be an important consideration in designing therapeutic strategies aimed at enhancing plasticity following TBI.

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“…Acoustic startle reflex has also been used to assess sensorimotor reactivity of a rat model of TBI (Wiley et al, 1996). At the same time, we evaluated the hearing condition following blast exposure at both peripheral and central levels using auditory brainstem responses (ABRs) and a prepulse inhibition (PPI) behavioral paradigm.…”

Section: Introductionmentioning

confidence: 99%

“…rats with fluid percussion-induced TBI (Wiley et al, 1996), but would equally affect all frequencies. To our knowledge, there are no studies that examined the effects of blast-induced tinnitus and hearing loss in rats.…”

mentioning

confidence: 99%

Blast-Induced Tinnitus and Hearing Loss in Rats: Behavioral and Imaging Assays

Mao

Pace

Pierozynski

et al. 2012

Journal of Neurotrauma

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The current study used a rat model to investigate the underlying mechanisms of blast-induced tinnitus, hearing loss, and associated traumatic brain injury (TBI). Seven rats were used to evaluate behavioral evidence of tinnitus and hearing loss, and TBI using magnetic resonance imaging following a single 10-msec blast at 14 psi or 194 dB sound pressure level (SPL). The results demonstrated that the blast exposure induced early onset of tinnitus and central hearing impairment at a broad frequency range. The induced tinnitus and central hearing impairment tended to shift towards high frequencies over time. Hearing threshold measured with auditory brainstem responses also showed an immediate elevation followed by recovery on day 14, coinciding with behaviorally-measured results. Diffusion tensor magnetic resonance imaging results demonstrated significant damage and compensatory plastic changes to certain auditory brain regions, with the majority of changes occurring in the inferior colliculus and medial geniculate body. No significant microstructural changes found in the corpus callosum indicates that the currently adopted blast exposure mainly exerts effects through the auditory pathways rather than through direct impact onto the brain parenchyma. The results showed that this animal model is appropriate for investigation of the mechanisms underlying blast-induced tinnitus, hearing loss, and related TBI. Continued investigation along these lines will help identify pathology with injury/recovery patterns, aiding development of effective treatment strategies.

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Reduced sensorimotor reactivity following traumatic brain injury in rats

Cited by 21 publications

References 23 publications

Metabolic, Neurochemical, and Histologic Responses to Vibrissa Motor Cortex Stimulation after Traumatic Brain Injury

Metabolic, Neurochemical, and Histologic Responses to Vibrissa Motor Cortex Stimulation after Traumatic Brain Injury

Use-Dependent Dendritic Regrowth Is Limited after Unilateral Controlled Cortical Impact to the Forelimb Sensorimotor Cortex

Blast-Induced Tinnitus and Hearing Loss in Rats: Behavioral and Imaging Assays

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