Comparative metabolic profiling of posterior parietal cortex, amygdala, and hippocampus in conditioned fear memory.
Comparative metabolic profiling of posterior parietal cortex, amygdala, and hippocampus in conditioned fear memory.
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条件性恐惧记忆中顶叶后皮质、杏仁核和海马体代谢的比较研究。
DOI：
10.1186/s13041-021-00863-x
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发表时间：
2021-10-06
期刊：
影响因子：
3.6
通讯作者：
Kim EK
中科院分区：
文献类型：
--
作者：
Jeon Y;Lim Y;Yeom J;Kim EK
Fear conditioning and retrieval are suitable models to investigate the biological basis of various mental disorders. Hippocampus and amygdala neurons consolidate conditioned stimulus (CS)-dependent fear memory. Posterior parietal cortex is considered important for the CS-dependent conditioning and retrieval of fear memory. Metabolomic screening among functionally related brain areas provides molecular signatures and biomarkers to improve the treatment of psychopathologies. Herein, we analyzed and compared changes of metabolites in the hippocampus, amygdala, and posterior parietal cortex under the fear retrieval condition. Metabolite profiles of posterior parietal cortex and amygdala were similarly changed after fear memory retrieval. While the retrieval of fear memory perturbed various metabolic pathways, most metabolic pathways that overlapped among the three brain regions had high ranks in the enrichment analysis of posterior parietal cortex. In posterior parietal cortex, the most perturbed pathways were pantothenate and CoA biosynthesis, purine metabolism, glutathione metabolism, and NAD+ dependent signaling. Metabolites of posterior parietal cortex including 4′-phosphopantetheine, xanthine, glutathione, ADP-ribose, ADP-ribose 2′-phosphate, and cyclic ADP-ribose were significantly regulated in these metabolic pathways. These results point to the importance of metabolites of posterior parietal cortex in conditioned fear memory retrieval and may provide potential biomarker candidates for traumatic memory-related mental disorders. The online version contains supplementary material available at 10.1186/s13041-021-00863-x.
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影响因子：
3.6
作者：
Joo, Bitna;Koo, Ja Wook;Lee, Sukwon
通讯作者：
Lee, Sukwon
影响因子：
16.6
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通讯作者：
HIRANO, T