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Hippocampal glutamate level and glutamate aspartate transporter (GLAST) are up-regulated in senior rat associated with isoflurane-induced spatial learning/memory impairment.
Neurochem Res 2013; 38(1):59-73NR

Abstract

Postoperative cognitive decline is a clinical concern especially for senior patients. It is generally recognized that glutamatergic system plays a crucial role in the physiopathologic process of neurocognitive deterioration. However, alterations of glutamatergic system in prolonged isoflurane-induced learning/memory decline are still unclear. This study investigates the question whether glutamate concentration and corresponding transporters or receptors display any alternations in aged rat suffering from isoflurane-induced learning/memory impairment. 111 male Sprague-Dawley rats (>18 months) were randomly divided into two main groups: hippocampal microdialysis group (n = 38) and western blotting group (n = 73). Each group was subdivided into three subgroups including (1) control subgroup (n = 6 and 10, receiving no behavioral trial, anesthesia or air exposure); (2) air-exposed subgroup (n = 7 and 15, receiving behavioral trial and air exposure but not anesthesia); (3) isoflurane anesthesia subgroup (n = 25 and 48, receiving both behavioral trial and anesthesia). The isoflurane-exposed rats were further divided into a learning/memory-impaired subgroup and a non-learning/memory-impaired subgroup according to their behavioral performance, which was measured using Morris water maze. Hippocampal glutamate concentrations in microdialysates were determined by high-performance liquid chromatography. Expression levels of GLAST, GLT-1, NMDAR1, NMDAR2A/B, AMPAR and tau in hippocampus were assessed via quantitative Western blotting. The incidences of learning/memory impairment of isoflurane-exposed rats in hippocampal microdialysis group and western blotting group were 12.0 (3/25) and 10.4 % (5/48) respectively. The intra-anesthesia hippocampal glutamate levels were significantly lower than those of non-anesthesized rats. The learning/memory-impaired rats showed a long-lasting increased glutamate level from 24 h after isoflurane exposure to the end of the study, but the other 22 isoflurane-exposed rats did not. The learning/memory-impaired subgroup displayed a significantly higher GLAST level than the other three subgroups (p = 0.026, 0.02 and 0.032 respectively). The expression levels of GLT-1, NMDAR1, NMDAR2A/B and AMPAR of every subgroup were comparable. We found a continuous raised hippocampal glutamate and an up-regulation of GLAST rather than GLT-1, NMDAR1, NMDAR2A/B, AMPAR or tau in hippocampus of aged rats associated with isoflurane-induced learning/memory impairment.

Authors+Show Affiliations

Beijing Chao-yang Hospital, Capital Medical University, Beijing, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23070469

Citation

Qu, Xiangdong, et al. "Hippocampal Glutamate Level and Glutamate Aspartate Transporter (GLAST) Are Up-regulated in Senior Rat Associated With Isoflurane-induced Spatial Learning/memory Impairment." Neurochemical Research, vol. 38, no. 1, 2013, pp. 59-73.
Qu X, Xu C, Wang H, et al. Hippocampal glutamate level and glutamate aspartate transporter (GLAST) are up-regulated in senior rat associated with isoflurane-induced spatial learning/memory impairment. Neurochem Res. 2013;38(1):59-73.
Qu, X., Xu, C., Wang, H., Xu, J., Liu, W., Wang, Y., ... Yue, Y. (2013). Hippocampal glutamate level and glutamate aspartate transporter (GLAST) are up-regulated in senior rat associated with isoflurane-induced spatial learning/memory impairment. Neurochemical Research, 38(1), pp. 59-73. doi:10.1007/s11064-012-0889-8.
Qu X, et al. Hippocampal Glutamate Level and Glutamate Aspartate Transporter (GLAST) Are Up-regulated in Senior Rat Associated With Isoflurane-induced Spatial Learning/memory Impairment. Neurochem Res. 2013;38(1):59-73. PubMed PMID: 23070469.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hippocampal glutamate level and glutamate aspartate transporter (GLAST) are up-regulated in senior rat associated with isoflurane-induced spatial learning/memory impairment. AU - Qu,Xiangdong, AU - Xu,Chengshi, AU - Wang,Hui, AU - Xu,Jie, AU - Liu,Weiran, AU - Wang,Yun, AU - Jia,Xingyuan, AU - Xie,Zhongcong, AU - Xu,Zhipeng, AU - Ji,Chao, AU - Wu,Anshi, AU - Yue,Yun, Y1 - 2012/10/16/ PY - 2012/06/10/received PY - 2012/09/10/accepted PY - 2012/08/31/revised PY - 2012/10/17/entrez PY - 2012/10/17/pubmed PY - 2013/5/31/medline SP - 59 EP - 73 JF - Neurochemical research JO - Neurochem. Res. VL - 38 IS - 1 N2 - Postoperative cognitive decline is a clinical concern especially for senior patients. It is generally recognized that glutamatergic system plays a crucial role in the physiopathologic process of neurocognitive deterioration. However, alterations of glutamatergic system in prolonged isoflurane-induced learning/memory decline are still unclear. This study investigates the question whether glutamate concentration and corresponding transporters or receptors display any alternations in aged rat suffering from isoflurane-induced learning/memory impairment. 111 male Sprague-Dawley rats (>18 months) were randomly divided into two main groups: hippocampal microdialysis group (n = 38) and western blotting group (n = 73). Each group was subdivided into three subgroups including (1) control subgroup (n = 6 and 10, receiving no behavioral trial, anesthesia or air exposure); (2) air-exposed subgroup (n = 7 and 15, receiving behavioral trial and air exposure but not anesthesia); (3) isoflurane anesthesia subgroup (n = 25 and 48, receiving both behavioral trial and anesthesia). The isoflurane-exposed rats were further divided into a learning/memory-impaired subgroup and a non-learning/memory-impaired subgroup according to their behavioral performance, which was measured using Morris water maze. Hippocampal glutamate concentrations in microdialysates were determined by high-performance liquid chromatography. Expression levels of GLAST, GLT-1, NMDAR1, NMDAR2A/B, AMPAR and tau in hippocampus were assessed via quantitative Western blotting. The incidences of learning/memory impairment of isoflurane-exposed rats in hippocampal microdialysis group and western blotting group were 12.0 (3/25) and 10.4 % (5/48) respectively. The intra-anesthesia hippocampal glutamate levels were significantly lower than those of non-anesthesized rats. The learning/memory-impaired rats showed a long-lasting increased glutamate level from 24 h after isoflurane exposure to the end of the study, but the other 22 isoflurane-exposed rats did not. The learning/memory-impaired subgroup displayed a significantly higher GLAST level than the other three subgroups (p = 0.026, 0.02 and 0.032 respectively). The expression levels of GLT-1, NMDAR1, NMDAR2A/B and AMPAR of every subgroup were comparable. We found a continuous raised hippocampal glutamate and an up-regulation of GLAST rather than GLT-1, NMDAR1, NMDAR2A/B, AMPAR or tau in hippocampus of aged rats associated with isoflurane-induced learning/memory impairment. SN - 1573-6903 UR - https://www.unboundmedicine.com/medline/citation/23070469/Hippocampal_glutamate_level_and_glutamate_aspartate_transporter__GLAST__are_up_regulated_in_senior_rat_associated_with_isoflurane_induced_spatial_learning/memory_impairment_ L2 - https://doi.org/10.1007/s11064-012-0889-8 DB - PRIME DP - Unbound Medicine ER -