Journal of neurotrauma
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Journal of neurotrauma · May 2010
Sensory stimulation prior to spinal cord injury induces post-injury dysesthesia in mice.
Chronic pain and dysesthesias are debilitating conditions that can arise following spinal cord injury (SCI). Research studies frequently employ rodent models of SCI to better understand the underlying mechanisms and develop better treatments for these phenomena. While evoked withdrawal tests can assess hypersensitivity in these SCI models, there is little consensus over how to evaluate spontaneous sensory abnormalities that are seen in clinical SCI subjects. ⋯ Mice subjected to either stimulus paradigm showed increased OG compared with unstimulated or uninjured mice. Histological analysis showed no difference in spinal cord lesion size due to sensory stimulation, or between mice that overgroomed or did not overgroom. The relationship between prior stimulation and contusion injury in mice that display OG indicates a critical interaction that may underlie one facet of spontaneous neuropathic symptoms after SCI.
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Journal of neurotrauma · May 2010
Blockade of acute microglial activation by minocycline promotes neuroprotection and reduces locomotor hyperactivity after closed head injury in mice: a twelve-week follow-up study.
Traumatic brain injury (TBI) causes a wide spectrum of consequences, such as microglial activation, cerebral inflammation, and focal and diffuse brain injury, as well as functional impairment. In this study we aimed to investigate the effects of acute treatment with minocycline as an inhibitor of microglial activation on cerebral focal and diffuse lesions, and on the spontaneous locomotor activity following TBI. The weight-drop model was used to induce TBI in mice. ⋯ More interestingly, minocycline significantly decreased TBI-induced locomotor hyperactivity at 48 h post-TBI, and its effect lasted for up to 8 weeks. Taken together, the results indicate that microglial activation appears to play an important role in the development of TBI-induced focal injury and the subsequent locomotor hyperactivity, and its short-term inhibition provides long-lasting functional recovery after TBI. These findings emphasize the fact that minocycline could be a promising new therapeutic strategy for head-injured patients.
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Journal of neurotrauma · May 2010
The effect of epidermal growth factor in the injured brain after trauma in rats.
Epidermal growth factor (EGF) is a known mitogen for neural stem and progenitor cells (NS/NPCs) in the central nervous system (CNS). In vitro, EGF maintains NS/NPCs in the proliferative state, whereas in the normal rodent brain it promotes their proliferation and migration in the subventricular zone (SVZ). Additionally, EGF administration can augment neuronal replacement in the ischemic-injured adult striatum. ⋯ Furthermore, we found that the EGF-induced proliferative population differentiated preferentially toward astroglial phenotype. Nevertheless, animals treated with EGF showed significant improvement in cognitive function, which was accompanied by reduced hippocampal neuronal cell loss. Collectively, the data from this study demonstrate that EGF exerts a neuroprotective rather than neurogenic effect in protecting the brain from injury.
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Journal of neurotrauma · May 2010
Prokineticin 2 expression is associated with neural repair of injured adult zebrafish telencephalon.
Prokineticin 2 (PROK2) is a secreted protein that regulates diverse biological processes including olfactory bulb neurogenesis in adult mammals. However, its precise role in this process is as yet not fully understood. Because it is well known that adult teleost fish, including zebrafish, display an intense proliferative activity in several brain regions, we took advantage of this feature to analyze the distribution of PROK2 transcripts in the adult zebrafish brain and during injury-induced telencephalon (TC) regeneration. ⋯ In addition, we observed a transient over-expression of PROK2 transcripts, which was detected in cells surrounding the lesion during the very first days post injury, and, a few days later, in broad cell rows extending from cortical regions of the TC toward injury sites. PROK2 over-expression was no longer detected when the regeneration process was close to completion, showing that ectopic PROK2 transcription paralleled neuronal regeneration. Taken together, our results suggest that in adult zebrafish brain, PROK2 may play a role in both constitutive and injury-induced neurogenesis.