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Sleep Deprivation Impairs Ca2+ Expression in the Hippocampus: Ionic Imaging Analysis for Cognitive Deficiency with TOF-SIMS

Published online by Cambridge University Press:  12 April 2012

Hung-Ming Chang
Affiliation:
Department of Anatomy, Faculty of Medicine, Chung Shan Medical University, Taichung 402, Taiwan Department of Pediatrics, Chung Shan Medical University Hospital, Taichung 402, Taiwan
Wen-Chieh Liao
Affiliation:
Department of Anatomy, Faculty of Medicine, Chung Shan Medical University, Taichung 402, Taiwan
Ji-Nan Sheu
Affiliation:
Department of Pediatrics, Chung Shan Medical University Hospital, Taichung 402, Taiwan
Chun-Chao Chang
Affiliation:
Department of Internal Medicine, Taipei Medical University Hospital, Taipei 110, Taiwan
Chyn-Tair Lan
Affiliation:
Department of Anatomy, Faculty of Medicine, Chung Shan Medical University, Taichung 402, Taiwan
Fu-Der Mai*
Affiliation:
Department of Biochemistry, School of Medicine, Taipei Medical University, Taipei 110, Taiwan Biomedical Mass Imaging Research Center, Taipei Medical University, Taipei 110, Taiwan
*
Corresponding author. E-mail: [email protected]
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Abstract

Sleep deprivation causes cognitive dysfunction in which impaired neuronal plasticity in hippocampus may underlie the molecular mechanisms of this deficiency. Considering calcium-mediated NMDA receptor subunit 1 (NMDAR1) and neuronal nitric oxide synthase (nNOS) activation plays an important role in the regulation of neuronal plasticity, the present study is aimed to determine whether total sleep deprivation (TSD) would impair calcium expression, together with injury of the neuronal plasticity in hippocampus. Adult rats subjected to TSD were processed for time-of-flight secondary ion mass spectrometry, NMDAR1 immunohistochemistry, nNOS biochemical assay, cytochrome oxidase histochemistry, and the Morris water maze learning test to detect ionic, neurochemical, bioenergetic as well as behavioral changes of neuronal plasticity, respectively. Results indicated that in normal rats, strong calcium signaling along with intense NMDAR1/nNOS expression were observed in hippocampal regions. Enhanced calcium imaging and neurochemical expressions corresponded well with strong bioenergetic activity and good performance of behavioral testing. However, following TSD, both calcium intensity and NMDAR1/nNOS expressions were significantly decreased. Behavioral testing also showed poor responses after TSD. As proper calcium expression is essential for maintaining hippocampal neuronal plasticity, impaired calcium expression would depress downstream NMDAR1-mediated nNOS activation, which might contribute to the initiation or development of TSD-related cognitive deficiency.

Type
Biological Applications
Copyright
Copyright © Microscopy Society of America 2012

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