The Journal of neuroscience : the official journal of the Society for Neuroscience
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Electrophysiological studies have established that the adult cerebral cortex undergoes immediate functional reorganizations after perturbations of the sensory periphery. These activity-dependent modifications are thought to be mediated via the rapid regulation of the synaptic strength of existing connections. Recent studies have implicated synaptic zinc as contributing to activity-dependent mechanisms of cortical plasticity, such as long-term potentiation and long-term depression, by virtue of its potent ability to modulate glutamatergic neurotransmission. ⋯ With longer survival times, levels of zinc staining gradually declined in deprived barrel hollows, returning to normal levels by 2-3 weeks after whisker removal. Increased levels of zinc staining in deprived barrel hollows were highly, negatively correlated with the length of whiskers as they regrew. These results indicate that levels of synaptic zinc in the neocortex are rapidly regulated by changes in sensory experience and suggest that zinc may participate in the plastic changes that normally occur in the cortex on a moment-to-moment basis.
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Lymphocytes respond to myelin proteins after spinal cord injury (SCI) and may contribute to post-traumatic secondary degeneration. However, there is increasing evidence that autoreactive T-lymphocytes may also convey neuroprotection and promote functional recovery after CNS injury. To clarify the role of myelin autoreactive lymphocytes after SCI, we performed contusion injuries in the thoracic spinal cord of transgenic (Tg) mice in which >95% of all CD4+ T-lymphocytes are reactive with myelin basic protein (MBP). ⋯ Any neuroprotection afforded by myelin-reactive T-cells is likely to be an indirect effect mediated by other non-CNS-reactive lymphocytes. Similar to the Tg mice in this study, a subset of humans that are genetically predisposed to autoimmune diseases of the CNS may be adversely affected by vaccine therapies designed to boost autoreactive lymphocyte responses after CNS trauma. Consequently, the safe implementation of such therapies requires that future studies define the mechanisms that control T-cell function within the injured CNS.
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Metabotropic glutamate receptor 5 (mGluR5) protein increased after sciatic nerve section in ipsilateral L4 and L5 DRG neuronal profiles, with most of the increase occurring in myelinated A-fiber somata. mGluR5 also increased in lamina II of the ipsilateral spinal cord and the proximal sciatic nerve stump in this model. After L5 spinal nerve ligation, mGluR5 immunoreactivity increased dramatically not only in damaged L5 but also in the neighboring undamaged L4. Interestingly, after partial sciatic nerve section, mGluR5 expression did not change in either L4 or L5 DRG neuronal profiles. ⋯ Furthermore, A-fibers in the uninjured L4 DRG after L5 spinal nerve ligation that have increased mGluR5 are the same A-fibers that newly express vanilloid receptor 1 after such injury. Together, these results suggest that, after L5 spinal nerve injury, mGluR5 expression on A-fibers is essential to the development of thermal hyperalgesia. After partial nerve section, however, it is unlikely that thermal responses are mediated through mGluR5 because no such increase in mGluR5 is detected in this model and MPEP is ineffective.