Journal of neurotrauma
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Journal of neurotrauma · Oct 2009
Electrical stimulation accelerates motor functional recovery in autograft-repaired 10 mm femoral nerve gap in rats.
Electrical stimulation has been shown to enhance peripheral nerve regeneration after nerve injury. However, the impact of electrical stimulation on motor functional recovery after nerve injuries, especially over long nerve gap lesions, has not been investigated in a comprehensive manner. In the present study, we aimed to determine whether electrical stimulation (1 h, 20 Hz) is beneficial for motor functional recovery after a 10 mm femoral nerve gap lesion in rats. ⋯ The rate of motor functional recovery was evaluated by single frame motion analysis and electrophysiological studies, and the nerve regeneration was investigated by double labeling and histological analysis. We found that brief electrical stimulation significantly accelerated motor functional recovery and nerve regeneration. Although the final outcome, both in functional terms and morphological terms, was not improved by electrical stimulation, the observed acceleration of functional recovery and axon regeneration may be of therapeutic importance in clinical setting.
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Journal of neurotrauma · Oct 2009
Heat stress preconditioning improves cognitive outcome after diffuse axonal injury in rats.
This study investigates the influence of heat stress preconditioning on cognitive outcome for rats with diffuse axonal injury (DAI), and attempts to examine the underlying mechanisms. Wistar rats were divided into four groups: rats subjected to heat stress preconditioning 24 h before induction of DAI (n = 10; HSDAI group), a DAI alone group (n = 10), a heat stress alone group (n = 10), and a sham-injury group (n = 10). From day 14 post-injury, the rats' learning abilities and memory were tested using the Morris water maze (MWM) task, followed by long-term potentiation (LTP) recording of the hippocampus. ⋯ Following injury, retraction balls, shrunken neurons, and HSP70 expression were visible in the brains of rats from the DAI and HSDAI groups; recovery was expedited in the rats belonging to the HSDAI group, as these pathological changes were alleviated, coincident with higher expression of HSP70. The rats' abilities for learning and memory were impaired following DAI; this may be due to the disconnection of brain regions, damage to neurons in the hippocampus, and a decrease in synaptic plasticity. Heat stress preconditioning is able to significantly attenuate this cognitive impairment, possibly mediated by the neuroprotective effect of HSP70.
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Journal of neurotrauma · Oct 2009
Molecular, anatomical, physiological, and behavioral studies of rats treated with buprenorphine after spinal cord injury.
Acute pain is a common symptom experienced after spinal cord injury (SCI). The presence of this pain calls for treatment with analgesics, such as buprenorphine. However, there are concerns that the drug may exert other effects besides alleviation of pain. ⋯ Microarray analysis demonstrated no significant difference in gene expression between rats treated with buprenorphine and the control group at 2 and 4 days post-injury (DPI). Experiments performed to determine the effect of buprenorphine at the electrophysiological (tcMMEP), behavioral (BBB, grid walking and beam crossing), and histological (luxol staining) levels revealed no significant difference at 7 and 14 DPI in the return of nerve conduction, functional recovery, or white matter sparing between control and experimental groups (p > 0.05, n = 6). These results show that buprenorphine (0.05 mg/kg) can be used as part of the postoperative care to reduce pain after SCI without affecting behavioral, physiological, or anatomical parameters.
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Journal of neurotrauma · Sep 2009
Traumatic injury activates MAP kinases in astrocytes: mechanisms of hypothermia and hyperthermia.
Hyperthermia is common following traumatic brain injury (TBI) and has been associated with poor neurologic outcome, and hypothermia has emerged as a potentially effective therapy for TBI, although its mechanism is still unclear. In this study we investigated the effects of temperature modulations on astrocyte survival following traumatic injury and the involved MAPK pathways. Trauma was produced by scratch injury of a monolayer of confluent astrocytes in culture, followed by incubation at hypothermia (308 degree C), normothermia (378 degree C), or hyperthermia (398 degree C). ⋯ Prolonged hyperthermia as a secondary insult worsens apoptosis by increasing JNK activation. Hypothermia protects against traumatic injury via early suppression on JNK activation and subsequent prevention of apoptosis. Manipulation of the JNK pathway in astrocytes may represent a therapeutic target for ameliorating the devastating progression of tissue injury and cell death after TBI.
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Journal of neurotrauma · Sep 2009
The persistent effects of concussion on neuroelectric indices of attention.
Mild traumatic brain injuries (mTBIs) that result from participation in sports are a major public health issue affecting 1.6-3.8 million individuals annually. The injury has been postulated as transient and void of long-term consequences when rapidly diagnosed and properly managed. Emerging evidence, however, has suggested an increased risk for late life cognitive dysfunction in those with previous injuries. ⋯ Significant decrements in the N2 and P3b amplitudes of the stimulus-locked ERP were noted for those with a history relative to those without a history of concussion. Although the previously concussed participants performed equal to those without injury on the clinical cognitive assessment, these findings support the notion that sport mTBI can no longer be thought of as a transient injury resulting in short-lived neurological impairment. It is not clear if these persistent deficits will manifest into clinical pathologies later in life.