Aim: To observe the effect of cholecystokinin (CCK) on lipofusin value, neuronal dendrite and spine ultrastructure, and total cellular protein during the process of experimental neuronal aging.
Methods: Experimental neuronal aging study model was established by NBA2 cellular serum-free culture method. By using single intracellular lipofusin value from microspectrophotometry, morphology of neuronal dendrites and spines from the scanner electron microscopy, and total cellular protein as the indexes of experimental neuronal aging, we observed the effect of CCK8 on the process of experimental neuronal aging.
Results: Under the condition of serum-free culture, intracellular fluorescence value (%) increased with the extension of culture time (1 d 8.51+/-3.43; 5 d 10.12+/-3.03; 10 d 20.54+/-10.3; 15 d 36.88+/-10.49; (b)P<0.01). When CCK was added to serum-free culture medium, intracellular lipofusin value (%) decreased remarkably after consecutive CCK reaction for 10 and 15 d (control 36.88+/-10.49; 5 d 32.03+/-10.01; 10 d 14.37+/-5.55; 15 d 17.31+/-4.80; (b)P<0.01). As the time of serum-free culturing was prolonged, the number of neuronal dendrite and spine cells decreased. The later increased in number when CCK8 was added. CCK8 could improve the total cellular protein in the process of experimental neuronal aging.
Conclusion: CCK8 may prolong the process of experimental neuronal aging by maintaining the structure and the number of neuronal dendrite and spine cells and changing the total cellular protein.
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http://dx.doi.org/10.3748/wjg.v11.i4.551 | DOI Listing |
PLoS One
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Department of Clinical Science, SUS, Division of Islet Cell Physiology, University of Lund, Malmö, Sweden.
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Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Hale Building for Transformative Medicine, Room 10006, 60 Fenwood Road, Boston, MA, 02115, USA.
α-Synuclein (αS) is a 140 amino-acid neuronal protein highly enriched in presynaptic nerve terminals. Its progressive accumulation in Lewy bodies and neurites is the hallmark of Parkinson's disease (PD). A growing number of studies highlights a critical interplay between lipid metabolism and αS biology.
View Article and Find Full Text PDFNeurol Int
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Department of Brain Repair & Rehabilitation, Institute of Neurology, University College London, London WC1E 6BT, UK.
The differential diagnosis of acute-onset amnesia includes transient global amnesia (TGA), transient epileptic amnesia (TEA), and functional (or psychogenic) amnesia. The most common of these, TGA, is a rare but well-described condition characterised by a self-limited episode of dense anterograde amnesia with variable retrograde amnesia. Although the clinical phenomenology of TGA is well described, its pathogenesis is not currently understood, thus preventing the development of evidence-based therapeutic recommendations.
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