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Activation of metabotropic glutamate receptor 1 regulates hippocampal ca1 region excitability in rats with status epilepticus by suppressing the HCN1 channel

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Neural Regeneration Research 2023年第3期18卷 594-602页

作者： Xiao-Dan Luo Tao Xiang Si-Jun Li Mei-Gang Ma Mei-Ling Chen Yuan Wu Department of Neurology First Affiliated Hospital of Guangxi Medical UniversityNanningGuangxi Zhuang Autonomous RegionChina Department of Neurology First Affiliated Hospital of University of South ChinaHengyangHunan ProvinceChina Department of Neurology Affiliated Hospital of Guilin Medical UniversityGuilinGuangxi Zhuang Autonomous RegionChina

Dysregulation of hyperpolarization-activated cyclic nucleotide-gated cation(HCN)channels alters neuronal ***,the role of HCN channels in status epilepticus is not fully *** this study,we established rat models of pentylenetetrazole-induced status *** performed western blot assays and immunofluorescence *** results showed that HCN1 channel protein expression,particularly HCN1 surface protein,was significantly decreased in the hippocampal ca1 region,whereas the expression of HCN2 channel protein was ***,metabolic glutamate receptor 1(mGluR1)protein expression was increased after status *** mGluR1 agonist(RS)-3,5-dihydroxyphenylglycine injected intracerebroventricularly increased the sensitivity and severity of pentylenetetrazole-induced status epilepticus,whereas application of the mGluR1 antagonist(+)-2-methyl-4-carboxyphenylglycine(LY367385)alleviated the severity of pentylenetetrazole-induced status *** results from double immunofluorescence labeling revealed that mGluR1 and HCN1 were co-localized in the ca1 ***,a protein kinase A inhibitor(H89)administered intraperitoneally successfully reversed HCN1 channel inhibition,thereby suppressing the severity and prolonging the latency of pentylenetetrazole-induced status ***,H89 reduced the level of mGluR1,downregulated cyclic adenosine monophosphate(caMP)/protein kinase A expression,significantly increased tetratricopeptide repeat-containing Rab8b-interacting protein(TRIP8b)(1a-4)expression,and restored TRIP8b(1b-2)***8b(1a-4)and TRIP8b(1b-2)are subunits of Rab8b interacting protein that regulate HCN1 surface protein.

关键词： (RS)-3,5-dihydroxyphenylglycine ca1 region excitability H89 HCN1 channel LY367385 mGluR1 pentylenetetrazole status epilepticus

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维普期刊数据库

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Therapeutic effect of bone marrow mesenchymal stem cells on cold stress induced changes in the hippocampus of rats

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Neural Regeneration Research 2014年第19期9卷 1740-1744页

作者： Saravana Kumar Sampath Kumar Saraswathi Perumal Vijayaraghavan Rajagopalan Department of Anatomy Saveetha Dental College Saveetha University ChennaiTamil NaduIndia

The present study aims to evaluate the effect of bone marrow mesenchymal stem cells on cold stress induced neuronal changes in hippocampal ca1 region of Wistar rats. Bone marrow mes- enchymal stem cells were isolated from a 6-week-old Wistar rat. Bone marrow from adult femora and tibia was collected and mesenchymal stem cells were cultured in minimal essential medium containing 10% heat-inactivated fetal bovine serum and were sub-cultured. Passage 3 cells were analyzed by flow cytometry for positive expression of CD44 and CD90 and negative expression of CD45. Once CD44 and CD90 positive expression was achieved, the cells were cultured again to 90% confluence for later experiments. Twenty-four rats aged 8 weeks old were randomly and evenly divided into normal control, cold water swim stress （cold stress）, cold stress ＋ PBS （intra- venous infusion）, and cold stress ＋ bone marrow mesenchymal stem cells （1 x 106; intravenous infusion） groups. The total period of study was 60 days which included 1 month stress period followed by 1 month treatment. Behavioral functional test was performed during the entire study period. After treatment, rats were sacrificed for histological studies. Treatment with bone marrow mesenchymal stem cells significantly increased the number of neuronal cells in hippocampal ca 1 region. Adult bone marrow mesenchymal stem cells injected by intravenous administration show potential therapeutic effects in cognitive decline associated with stress-related lesions.

关键词： nerve regeneration bone marrow mesenchymal stem cells hippocampus cold stress intravenous cognition neuronal cells ca1 region neural regeneration

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维普期刊数据库

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Effects of electroacupuncture on microcirculatory blood flow and glucose transporter function in the hippocampus

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Neural Regeneration Research 2011年第3期6卷 200-205页

作者： Lu, Yan Han, Bingbing Wang, Shijun Shandong Univ Tradit Chinese Med Dept Expt Acupuncturol Acupuncture & Moxibust Coll Jinan 250355 Shandong Peoples R China Shandong Univ Tradit Chinese Med Microcirculat Lab Basic Med Coll Jinan 250355 Shandong Peoples R China

Nerve cell metabolism in post brain ischemia depends on increased microcirculation perfusion and transport function of microvascular endothelial cells. In the present study, a rat model of middle cerebral artery occlusion was established to investigate the influence of electroacupuncture （EA） on hippocampal ca1 cerebral blood flow and glucose transporter 1 （GLUT1） expression in the microvascular endothelial cells. Following EA at Neiguan （PC 6）, the cerebral blood flow in the ischemic hippocampal ca1 region was significantly elevated, the number and microvascular integrated absorbance of the GLUTl-positive cells were significantly increased, nerve cell damage was ameliorated, and GLUT1 protein expression in the ischemic hippocampus was significantly increased. Results demonstrate that EA increased the cerebral blood flow of the hippocampal ca1 region and improved the glucose transport function, thereby attenuating neuronal injuries.

关键词： Electroacupuncture Neiguan (PC 6) focal cerebral ischemia microvascularendothelial cells glucose transporter 1 cerebral blood flow ca1 region neural regeneration

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Delayed hippocampal neuronal death in young gerbil following transient global cerebral ischemia is related to higher and longer-term expression of p63 in the ischemic hippocampus

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Neural Regeneration Research 2015年第6期10卷 944-950页

作者： Eun Joo Bae Bai Hui Chen Bing Chun Yan Bich Na Shin Jeong Hwi Cho In Hye Kim Ji Hyeon Ahn Jae Chul Lee Hyun-Jin Tae Seongkweon Hong Dong Won Kim Jun Hwi Cho Yun Lyul Lee Moo-Ho Won Joon Ha Park Department of Pediatrics Chuncheon Sacred Heart HospitalCollege of MedicineHallym University Department of Physiology College of MedicineInstitute of Neurodegeneration and NeuroregenerationHallym University Institute of Integrative Traditional & Western Medicine Medical CollegeYangzhou University Department of Neurobiology School of MedicineKangwon National University Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym University Department of Surgery School of MedicineKangwon National University Department of Emergency Medicine Chuncheon Sacred Heart HospitalCollege of MedicineHallym University Department of Emergency Medicine School of MedicineKangwon National University

The tumor suppressor p63 is one of p53 family members and plays a vital role as a regulator of neuronal apoptosis in the development of the nervous system. However, the role of p63 in mature neuronal death has not been addressed yet. In this study, we first compared ischemia-induced effects on p63 expression in the hippocampal regions （ca1-3） between the young and adult gerbils subjected to 5 minutes of transient global cerebral ischemia. Neuronal death in the hippocampal ca1 region of young gerbils was significantly slow compared with that in the adult gerbils after transient global cerebral ischemia, p63 immunoreactivity in the hippocampal ca1 pyramidal neurons in the sham-operated young group was significantly low compared with that in the sham-operated adult group, p63 immunoreactivity was apparently changed in ischemic hippocampal ca1 pyramidal neurons in both ischemia-operated young and adult groups. In the ischemia-operated adult groups, p63 immunoreactivity in the hippocampal ca1 pyramidal neurons was significantly decreased at 4 days post-ischemia; however, p63 immunoreactivity in the ischemia-operated young group was significantly higher than that in the ischemia-operated adult group. At 7 days post-ischemia, p63 immunoreactivity was decreased in the hippocampal ca1 pyramidal neurons in both ischemia-operated young and adult groups. Change patterns of p63 level in the hippocampal ca1 region of adult and young gerbils after ischemic damage were similar to those observed in the immunohistochemical results. These findings indicate that higher and longer-term expression of p63 in the hippocampal ca1 region of the young gerbils after ischemia/reperfusion may be related to more delayed neuronal death compared to that in the adults.

关键词： p53 tumor suppressor gene family cerebral ischemia/reperfusion pyramidal neurons ca1 region delayed neuronal death immunohistochemistry western blotting neural regeneration

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