Rev Neuroscience
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Migraine is the most common neurologic condition. One-third of migraineurs experience transient neurologic symptoms, the so-called aura. There is strong evidence that spreading depression (SD) is the electrophysiologic substrate of migraine aura. ⋯ S218L mice display additional signs such as seizures and coma when SD propagates into hippocampus and thalamus. In hyperexcitable FHM brains, SD may propagate between cortex and subcortical structures via permissive gray matter bridges, or originate de novo in subcortical structures, to explain unusual and severe aura signs and symptoms. Reciprocal spread and reverberating waves can explain protracted attacks.
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During the last two decades, it became increasingly evident that glial cells accomplish a more important role in brain function than previously thought. Glial cells express pannexins and connexins, which are member subunits of two protein families that form membrane channels termed hemichannels. These channels communicate intra- and extracellular compartments and allow the release of autocrine/paracrine signaling molecules [e.g., adenosine triphosphate (ATP), glutamate, nicotinamide adenine dinucleotide, and prostaglandin E2] to the extracellular milieu, as well as the uptake of small molecules (e.g., glucose). ⋯ Because ATP and glutamate are released via glial hemichannels in neurodegenerative conditions, it is expected that they contribute to neurotoxicity. More importantly, toxic molecules released via glial hemichannels could increase the Ca2+ entry in neurons also via neuronal hemichannels, leading to neuronal death. Therefore, blockade of hemichannels expressed by glial cells and/or neurons during neuroinflammation might prevent neurodegeneration.
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The default mode network (DMN) is a unique idea that attracts many neuroimaging researchers to examine alterations in the resting-state brain physiology in normal aging and psychiatric and neurological disorders predominantly by using functional magnetic resonance imaging (fMRI). In dementias, especially in Alzheimer's disease (AD), one of the recent topics in an imaging domain is depicting its pathological substance, β-amyloid protein (Aβ) in vivo using positron emission tomography (PET). This Aβ accumulation was not only discovered in AD but also frequently in cognitively normal people. ⋯ Our recent study of the cognitive and physiological impact of Aβ accumulation on the DMN function in normal elderly people using PET has shown that the amount of Aβ deposits is negatively correlated with the DMN function, and the lower function of the DMN is associated with poorer working memory performance. As expected, Aβ deposition in the brain, however minute the degree of its accumulation can be, may cause neuronal discoordination in the DMN along with poor working memory in normal aging. As literature on fMRI-based DMN activity is profuse, here, we discuss the pathophysiological aspect of the DMN from a molecular imaging viewpoint.
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Recent therapeutic human studies testing transcranial direct current stimulation (tDCS) has shown promising results, although many questions remain unanswered. Translational research with experimental animals is an appropriate framework for investigating its mechanisms of action that are still undetermined. Nevertheless, animal and human studies are often discordant. ⋯ Nonetheless, almost all studies demonstrated that tDCS had positive immediate and long-lasting effects. Vis-à-vis human trials, animal studies applied higher current densities (34.2 vs. 0.4 A/m(2), respectively), preferred extra-cephalic positions for reference electrodes (60% vs. 10%, respectively) and used electrodes with different sizes more often. Potential implications for translational tDCS research are discussed.
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We have reviewed the literature on transcranial magnetic stimulation studies in patients with brain death, coma, vegetative, minimally conscious, and locked-in states. Transcranial magnetic stimulation permits non-invasive study of brain excitability and may extend our understanding of the underlying mechanisms of these disorders. However, use of this technique in severe brain damage remains methodologically ill-defined and must be further validated prior to clinical application in these challenging patients.