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      N-Butylphthalide Improves Cognitive Function in Rats after Carbon Monoxide Poisoning.

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          Abstract

          Cognitive impairment is the most common neurologic sequelae after carbon monoxide (CO) poisoning, and the previous investigations have demonstrated that N-Butylphthalide (NBP) could exert a broad spectrum of neuroprotective properties. The current study aimed to investigate the effect of NBP on cognitive dysfunction in rats after acute severe CO poisoning. Rats were randomly divided into a normal control group, a CO poisoning group and a CO+NBP group. The animal model of CO poisoning was established by exposure to CO in a chamber, and then all rats received hyperbaric oxygen therapy once daily, while rats in CO+NBP group were administered orally NBP (6 mg/ 100g) by gavage twice a day additionally. The results indicated that CO poisoning could induce cognitive impairment. The ultrastructure of hippocampus was seriously damaged under transmission electron microscopy, and the expressions of calpain 1 and CaMK II proteins were significantly elevated after CO exposure according to the analysis of immunofluorescence staining and western blot. NBP treatment could evidently improve cognitive function, and maintain ultrastructure integrity of hippocampus. The expression levels of both calpain 1 and CaMK II proteins in CO+NBP group were considerably lower than that of CO poisoning group (P < 0.05). Taken together, this study highlights the molecular mechanism of cognitive dysfunction in rats after CO exposure via the upregulation of both calpain 1 and CaMK II proteins. The administration of NBP could balance the expressions of calpain 1 and CaMK II proteins and improve cognitive function through maintaining ultrastructural integrity of hippocampus, and thus may play a neuroprotective role in brain tissue in rats with CO poisoning.

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          Autophosphorylation at Thr286 of the alpha calcium-calmodulin kinase II in LTP and learning.

          N. Fedorov, K Giese, R K Filipkowski … (1998)
          The calcium-calmodulin-dependent kinase II (CaMKII) is required for hippocampal long-term potentiation (LTP) and spatial learning. In addition to its calcium-calmodulin (CaM)-dependent activity, CaMKII can undergo autophosphorylation, resulting in CaM-independent activity. A point mutation was introduced into the alphaCaMKII gene that blocked the autophosphorylation of threonine at position 286 (Thr286) of this kinase without affecting its CaM-dependent activity. The mutant mice had no N-methyl-D-aspartate receptor-dependent LTP in the hippocampal CA1 area and showed no spatial learning in the Morris water maze. Thus, the autophosphorylation of alphaCaMKII at Thr286 appears to be required for LTP and learning.
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            Brain indoleamine 2,3-dioxygenase contributes to the comorbidity of pain and depression.

            Hyangin Kim, Lucy Chen, Grewo Lim … (2012)
            Pain and depression are frequently comorbid disorders, but the mechanism underlying this association is unknown. Here, we report that brain indoleamine 2,3-dioxygenase 1 (IDO1), a rate-limiting enzyme in tryptophan metabolism, plays a key role in this comorbidity. We found that chronic pain in rats induced depressive behavior and IDO1 upregulation in the bilateral hippocampus. Upregulation of IDO1 resulted in the increased kynurenine/tryptophan ratio and decreased serotonin/tryptophan ratio in the bilateral hippocampus. We observed elevated plasma IDO activity in patients with both pain and depression, as well as in rats with anhedonia induced by chronic social stress. Intra-hippocampal administration of IL-6 in rats, in addition to in vitro experiments, demonstrated that IL-6 induces IDO1 expression through the JAK/STAT pathway. Further, either Ido1 gene knockout or pharmacological inhibition of hippocampal IDO1 activity attenuated both nociceptive and depressive behavior. These results reveal an IDO1-mediated regulatory mechanism underlying the comorbidity of pain and depression and suggest a new strategy for the concurrent treatment of both conditions via modulation of brain IDO1 activity.
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              Hippocampal size predicts rapid learning of a cognitive map in humans.

              Victor Schinazi, Daniele Nardi, Nora Newcombe … (2013)
              The idea that humans use flexible map-like representations of their environment to guide spatial navigation has a long and controversial history. One reason for this enduring controversy might be that individuals vary considerably in their ability to form and utilize cognitive maps. Here we investigate the behavioral and neuroanatomical signatures of these individual differences. Participants learned an unfamiliar campus environment over a period of three weeks. In their first visit, they learned the position of different buildings along two routes in separate areas of the campus. During the following weeks, they learned these routes for a second and third time, along with two paths that connected both areas of the campus. Behavioral assessments after each learning session indicated that subjects formed a coherent representation of the spatial structure of the entire campus after learning a single connecting path. Volumetric analyses of structural MRI data and voxel-based morphometry (VBM) indicated that the size of the right posterior hippocampus predicted the ability to use this spatial knowledge to make inferences about the relative positions of different buildings on the campus. An inverse relationship between gray matter volume and performance was observed in the caudate. These results suggest that (i) humans can rapidly acquire cognitive maps of large-scale environments and (ii) individual differences in hippocampal anatomy may provide the neuroanatomical substrate for individual differences in the ability to learn and flexibly use these cognitive maps. © 2013 Wiley Periodicals, Inc.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Front Pharmacol
                Title: Frontiers in pharmacology
                Publisher: Frontiers Media SA
                ISSN: 1663-9812
                ISSN (Print): 1663-9812
                Publication date (Electronic): 2017
                Volume: 8
                Affiliations
                [1 ] Department of Integration of Chinese and Western Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao UniversityYantai, China; Emergency Centre, The Affiliated Yantai Yuhuangding Hospital of Qingdao UniversityYantai, China.
                [2 ] Emergency Centre, The Affiliated Yantai Yuhuangding Hospital of Qingdao University Yantai, China.
                [3 ] Department of Integration of Chinese and Western Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao University Yantai, China.
                [4 ] Department of Integration of Chinese and Western Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao UniversityYantai, China; Department of Integration of Chinese and Western Clinical Medicine, Qingdao University Medical CollegeQingdao, China.
                [5 ] The Second Clinical Medical College, Shandong University of Traditional Chinese Medicine Jinan, China.
                [6 ] Department of Clinical Medicine, Binzhou Medical University Yantai, China.
                [7 ] Eye Institute, Shandong University of Traditional Chinese Medicine Jinan, China.
                Article
                DOI: 10.3389/fphar.2017.00064
                PMC ID: 5298996
                PubMed ID: 28232802
                SO-VID: 5ca5b833-1a45-4777-af45-86d88c423869
                History

                Keywords: CO poisoning,Ca2+/calmodulin dependent protein kinase II,Calpain 1,N-butylphthalide,cognitive function,rat
                Data availability:
                Keywords: CO poisoning, Ca2+/calmodulin dependent protein kinase II, Calpain 1, N-butylphthalide, cognitive function, rat

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