Rev Neuroscience
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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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Randomized Controlled Trial
Glucocorticoid-endocannabinoid interaction in cardiac surgical patients: relationship to early cognitive dysfunction and late depression.
Endocannabinoids (ECs) are rapidly acting immune-modulatory lipid-signaling molecules that are important for adaptation to stressful and aversive situations.They are known to interact with glucocorticoids and other stress-responsive systems. Maladaptation to acute or chronic stress represents a major risk factor for the development of psychiatric disorders. In the present study, we administered stress doses of hydrocortisone ina prospective, randomized, placebo-controlled double blind study in patients undergoing cardiac surgery (CS) to examine the relationship between the use of glucocorticoids, plasma EC levels, and the occurrence of early postoperative cognitive dysfunction (delirium) and of later development of depression. ⋯ A low perioperative EC response may indicate an increased risk for early cognitive dysfunction and long-term depression in patients after CS. Glucocorticoids do not seem to influence this relationship.
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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.