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Protein Kinase C Controls the Excitability of Cortical pyramidal neurons by Regulating Kv2.2 Channel Activity

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Neuroscience Bulletin 2022年第2期38卷 135-148页

作者： Zhaoyang Li Wenhao Dong Xinyuan Zhang Jun-Mei Lu Yan-Ai Mei Changlong Hu State Key Laboratory of Medical Neurobiology Institutes of Brain Science and School of Life SciencesFudan UniversityShanghai 200438China

The family of voltage-gated potassium Kv2 channels consists of the Kv2.1 and Kv2.2 subtypes.Kv2.1 is constitutively highly phosphorylated in neurons and its function relies on its phosphorylation state.Whether the function of Kv2.2 is also dependent on its phosphorylation state remains unknown.Here,we investigated whether Kv2.2 channels can be phosphorylated by protein kinase C(PKC)and examined the effects of PKC-induced phosphorylation on their activity and function.Activation of PKC inhibited Kv2.2 currents and altered their steadystate activation in HEK293 cells.Point mutations and specific antibodies against phosphorylated S481 or S488 demonstrated the importance of these residues for the PKC-dependent modulation of Kv2.2.In layer Ⅱ pyramidal neurons in cortical slices,activation of PKC similarly regulated native Kv2.2 channels and simultaneously reduced the frequency of action potentials.In conclusion,this study provides the first evidence to our knowledge that PKC-induced phosphorylation of the Kv2.2 channel controls the excitability of cortical pyramidal neurons.

关键词： Kv2.2 PKC Phosphorylation pyramidal neurons Excitability

Regulation of specific abnormal calcium signals in the hippocampal CA1 and primary cortex M1 alleviates the progression of temporal lobe epilepsy

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Neural Regeneration Research 2024年第2期19卷 425-433页

作者： Feng Chen Xi Dong Zhenhuan Wang Tongrui Wu Liangpeng Wei Yuanyuan Li Kai Zhang Zengguang Ma Chao Tian Jing Li Jingyu Zhao Wei Zhang Aili Liu Hui Shen Laboratory of Neurobiology School of Biomedical EngineeringTianjin Medical UniversityTianjinChina Institute for Translational Neuroscience the Second Affiliated Hospital of Nantong UniversityNantongJiangsu ProvinceChina Institute for Translational Brain Research Fudan UniversityShanghaiChina Department of Radiology the Affiliated Drum Tower Hospital of Nanjing University Medical SchoolNanjingJiangsu ProvinceChina Innovative Institute of Chinese Medicine and Pharmacy Shandong University of Traditional Chinese MedicineJinanChina Department of Anesthesiology Tianjin Medical University General HospitalTianjinChina Department of Orthopaedics Tianjin Medical University General HospitalTianjinChina Tianjin Eye Hospital Tianjin Eye InstituteTianjin Key Lab of Ophthalmology and Visual ScienceTianjinChina Laboratory of Neurobiology School of Basic Medical SciencesTianjin Medical UniversityTianjinChina

Temporal lobe epilepsy is a multifactorial neurological dysfunction syndrome that is refractory,resistant to antiepileptic drugs,and has a high recurrence rate.The pathogenesis of temporal lobe epilepsy is complex and is not fully understood.Intracellular calcium dynamics have been implicated in temporal lobe epilepsy.However,the effect of fluctuating calcium activity in CA1 pyramidal neurons on temporal lobe epilepsy is unknown,and no longitudinal studies have investigated calcium activity in pyramidal neurons in the hippocampal CA1 and primary motor cortex M1 of freely moving mice.In this study,we used a multichannel fiber photometry system to continuously record calcium signals in CA1 and M1 during the temporal lobe epilepsy process.We found that calcium signals varied according to the grade of temporal lobe epilepsy episodes.In particular,cortical spreading depression,which has recently been frequently used to represent the continuously and substantially increased calcium signals,was found to correspond to complex and severe behavioral characteristics of temporal lobe epilepsy ranging from gradeⅡto gradeⅤ.However,vigorous calcium oscillations and highly synchronized calcium signals in CA1 and M1 were strongly related to convulsive motor seizures.Chemogenetic inhibition of pyramidal neurons in CA1 significantly attenuated the amplitudes of the calcium signals corresponding to gradeⅠepisodes.In addition,the latency of cortical spreading depression was prolonged,and the above-mentioned abnormal calcium signals in CA1 and M1 were also significantly reduced.Intriguingly,it was possible to rescue the altered intracellular calcium dynamics.Via simultaneous analysis of calcium signals and epileptic behaviors,we found that the progression of temporal lobe epilepsy was alleviated when specific calcium signals were reduced,and that the end-point behaviors of temporal lobe epilepsy were improved.Our results indicate that the calcium dynamic between CA1 and M1 may reflect specific epileptic behaviors corresponding to diff

关键词： Ca^(2+) calcium signals chemogenetic methods hippocampus primary motor cortex pyramidal neurons temporal lobe epilepsy

Effect of etomidate on voltage-dependent potassium currents in rat isolated hippocampal pyramidal neurons

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Chinese Medical Journal 2010年第6期123卷 702-706页

作者： TAN Hong-yu SUN Li-na WANG Xiao-liang YE Tie-hu Key Laboratory of Carcinogenesis and Translational Research Ministry of Education Department of AnesthesiologyPeking University School of OncologyBeijing Cancer Hospital & InstituteBeijing 100142China Department of Anesthesiology Peking Union Medical College HospitalChinese Academy of Medical Sciences & Peking Union Medical CollegeBeijing 100730China Department of Pharmacology Capital Medical UniversityBeijing 100069China Department of Pharmacology Institute of Materia MedicaChinese Academy of Medical Sciences & Peking Union Medical CollegeBeijing 100730China

Background Previous studies demonstrated general anesthetics affect potassium ion channels, which may be one of the mechanisms of general anesthesia. Because the effect of etomidate on potassium channels in rat hippocampus which is involved in memory function has not been studied, we investigated the effects of etomidate on both delayed rectifier potassium current （IK（DR）） and transient outward potassium current （I_K（A）） in acutely dissociated rat hippocampal pyramidal neurons.Methods Single rat hippocampal pyramidal neurons from male Wistar rats of 7-10 days were acutely dissociated by enzymatic digestion and mechanical dispersion according to the methods of Kay and Wong with slight modification. Voltage-clamp recordings were performed in the whole-cell patch clamp configuration. Currents were recorded with a List EPC-10 amplifier and data were stored in a computer using Pulse 8.5. Student＇s paired two-tail t test was used for data analysis. Results At the concentration of 100 μmol/L, etomidate significantly inhibited IK（DR） by 49.2% at ＋40 mV when depolarized from -110 mV （P 〈0.01, n=8）, while did not affect IK（A）（/1=8, P 〉0.05）. The IC50value of etomidate for blocking IK（DR）was calculated as 5.4 μmol/L, with a Hill slope of 2.45. At the presence of 10 μmol/L etomidate, the V1/2 of activation curve was shifted from （17.3±1.5） mV to （10.7±9.9） mV （n=8, P 〈0.05）, the V1/2 of inactivation curve was shifted from （-18.3±2.2） mV to （-45.3±9.4） mV （n=8, P 〈0.05）. Etomidate 10 μmol/L shifted both the activation curve and inactivation curve of IK（DR））to negative potential, but mainly affected the inactivation kinetics.Conclusions Etomidate potently inhibited IK（DR） but not IK（A） in rat hippocampal pyramidal neurons. IK（DR） was inhibited by etomidate in a concentration-dependent manner, while IK（A） remained unaffected.

关键词： etomidate hippocampus pyramidal neurons patch clamp potassium currents

Neuroprotection of Chrysanthemum indicum Linne against cerebral ischemia/reperfusion injury by anti-inflammatory effect in gerbils

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Neural Regeneration Research 2016年第2期11卷 270-277页

作者： Ki-YeonYoo In Hye Kim Jeong-Hwi Cho li Hyeon Ahn Joon Ha Park Jae-Chul Lee Hyun-Jin Tae Dae Won Kim Jong-Dai Kim Seongkweon Hong Moo-Ho Won il Jun Kang Department of Oral Anatomy College of Dentistry and Research Institute of Oral Science Gangneung-Wonju National University GangneungRepublic of Korea Department of Neurobiology School of Medicine Kangwon National University Chuncheon Republic of Korea Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Chuncheon Republic of Korea Department of Biochemistry and Molecular Biology College of Dentistry and Research Institute of Oral Science Gangneung-Wonju NationalUniversity Gangneung Republic of Korea Division of Food Biotechnology School of Biotechnology Kangwon National University Chuncheon Republic of Korea Department of Surgery School of Medicine Kangwon National University Chuncheon Republic of Korea Department of Food Science and Nutrition Hallym University Chuncheon Republic of Korea

In this study, we tried to verify the neuroprotective effect of Chrysanthemum indicum Linne（CIL） extract, which has been used as a botanical drug in East Asia, against ischemic damage and to explore the underlying mechanism involving the anti-inflammatory approach. A gerbil was given CIL extract for 7 consecutive days followed by bilateral carotid artery occlusion to make a cerebral ischemia/reperfusion model. Then, we found that CIL extracts protected pyramidal neurons in the hippocampal CA1 region（CA1） from ischemic damage using neuronal nucleus immunohistochemistry and Fluoro-Jade B histofluorescence. Accordingly, interleukin-13 immunoreactivities in the CA1 pyramidal neurons of CIL-pretreated animals were maintained or increased after cerebral ischemia/reperfusion. These findings indicate that the pre-treatment of CIL can attenuate neuronal damage/death in the brain after cerebral ischemia/reperfusion via an anti-inflammatory approach.

关键词： nerve regeneration transient cerebral ischemia delayed neuronal death pyramidal neurons inflammatory cytokines neural regeneration

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

Pretreated Glehnia littoralis Extract Prevents Neuronal Death Following Transient Global Cerebral Ischemia through Increases of Superoxide Dismutase 1 and Brain-derived Neurotrophic Factor Expressions in the Gerbil Hippocampal Cornu Ammonis 1 Area

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Chinese Medical Journal 2017年第15期130卷 1796-1803页

作者： Joon Ha Park Tae-Kveono Lee Bing-Chun Yan Bich-Na Shin Ji Hyeon Ahn In Hye Kim Jeong Hwi Cho Jae-Chul Lee In Koo Hwang Jong Dai Kim Seongkweon Hong Young Joo Lee Moo-Ho Woll Il Jun Kang Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Chuncheon 24252 Korea Department of Neurobiology School of Medicine Kangwon National University Chuncheon 24341 Korea Department of Traditional Chinese and Western Medicine Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases Yangzhou Jiangsu 225001 China Department of Physiology College of Medicine Hallym University Chuncheon 24252 Korea Department of Anatomy and Cell Biology College of Veterinary Medicine and Research Institute for Veterinary Science Seoul National University Seoul08826 Korea Division of Food Biotechnology School of Biotechnology Kangwon National University Chuncheon 24341 Korea Department of Surgery School of Medicine Kangwon National University Chuncheon 24341 Korea Department of Emergency Medicine Seoul Hospital College of Medicine Sooncheonhyang University Seoul 04401 Korea Department of Food Science and Nutrition Hallym University Chuncheon 24252 Korea

Background：Glehnia littoralis,as a traditional herbal medicine to heal various health ailments in East Asia,displays various therapeutic properties including antioxidant effects.However,neuroprotective effects of G.littoralis against cerebral ischemic insults have not yet been addressed.Therefore,in this study,we first examined its neuroprotective effects in the hippocampus using a gerbil model of transient global cerebral ischemia （TGCI）.Methods：Gerbils were subjected to TGCI for 5 min.G.littoralis extract （GLE;100 and 200 mg/kg） was administrated orally once daily for 7 days before ischemic surgery.Neuroprotection was examined by neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining.Gliosis was observed by immunohistochemistry for glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1.For neuroprotective mechanisms,immunohistochemistry for superoxide dismutase （SOD） 1 and brain-derived neurotrophic factor （BDNF） was done.Results：Pretreatment with 200 mg/kg of GLE protected pyramidal neurons in the cornu ammonis 1 （CA1） area from ischemic insult area （F=29.770,P 〈 0.05） and significantly inhibited activationsof astrocytes （F =22.959,P 〈 0.05） and microglia （F =44.135,P 〈 0.05） in the ischemic CA1 area.In addition,pretreatment with GLE significantly increased expressions of SOD1 （F =28.561,P 〈 0.05） and BDNF （F =55.298,P 〈 0.05） in CA1 pyramidal neurons of the sham-and ischemia-operated groups.Conclusions：Our findings indicate that pretreatment with GLE can protect neurons from ischemic insults,and we suggest that its neuroprotective mechanism may be closely associated with increases of SOD 1 and BDNF expressions as well as attenuation ofglial activation.

关键词： Antioxidant Gtial Activation Neurotrophic Factor Neuroprotection pyramidal neurons

Hippocampal CA1 pyramidal cells and neurotrophic factors in a rat model of vascular dementia following Xiongma drop pill versus Ginkgo leaf tablets

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Neural Regeneration Research 2009年第12期4卷 973-978页

作者： Ying Zhao Lin Liu Houjun Teng Jiling Jiang Dan Li College of Pharmacy Harbin University of Commerce Harbin 150076 Heilongjiang Province China

BACKGROUND： Previous studies have demonstrated the neuroprotective effects of Xiongma drop pill （XMDP） in a mouse model of vascular dementia. Neurotrophic factors play an important role in repair and regeneration of injured neurons. OBJECTIVE： To compare the effects of XMDP and Ginkgo leaf tablets on the appearance and number of hippocampal CA1 pyramidal neurons, as well as neurotrophic factor content in brain tissues, during vascular dementia formation to explore the neuroprotective mechanisms of XMDP. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Laboratory of Pharmacology, College of Pharmacy, Harbin University of Commerce between April 2007 and December 2008. MATERIALS： XMDP was prepared by the College of Pharmacy, Harbin University of Commerce, with each 40 mg pill containing ferulic acid （≥ 0.149 mg） and gastrodin （≥ 0.171 mg）. Ginkgo leaf tablets were purchased from Taiyuan Qianyuan Pharmacy, China. METHODS： Healthy, adult, male, Wistar rats were randomly assigned to 6 groups： sham-operation, model, XMDP （high-, middle-, and low- dose）, and Ginkgo leaf tablets. The 6 groups were subdivided into two subgroups according to administration days, i.e., 30 and 60 days, with 8 animals in each subgroup. Rats in the model, XMDP, and Ginkgo leaf tablets groups were subjected to permanent bilateral ligation of the common carotid artery to establish a vascular dementia model. At 8 days after model establishment, all groups received intragastric administration once daily of the following： 10 mL/kg normal saline in the sham-operation and model groups; 0.4, 0.2, and 0.1 g/kg XMDP in the high-, middle-, and low-dose XMDP groups, respectively; and 50 mg/kg Ginkgo leaf tablets in the Ginkgo leaf tablets group. MAIN OUTCOME MEASURES： Hematoxylin-eosin staining was used to observe appearance and to quantify the number of hippocampal CA1 pyramidal neurons. Brain-derived neurotrophic factor and nerve growth factor concentrations in brain tissues were detected by enzyme-linked immunos

关键词： Xiongma drop pill vascular dementia pyramidal neurons brain-derived neurotrophic factor nerve growth factor

Advances in genomic study of cortical projection neurons

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Frontiers in Biology 2010年第6期5卷 524-531页

作者： Chunsheng QU Jieguang CHEN Key Laboratory of Visual Science National Ministry of Healthand School of Optometry and OphthalmologyWenzhou Medical CollegeZhejiang 325027China.

The mammalian neocortex gives rise to perception and initiates voluntary motor responses.The cortical laminae are comprised of six distinct cellular layers of local circuit neurons and projection neurons.To explore molecular identities of the distinct cortical projection neurons,discovery-orientated genomic approaches have been adopted.Microarray analysis of dissected cortical tissues has been applied to identify cortical layer markers.Early neuronal cells were sorted by FACS from GFP-labeled embryonic brains for gene expression proﬁling.Laser capture microdissection of retrograde-labeled pro-jection neurons,when coupled with optimal RNA ampliﬁcation technology,has become a valuable strategy for neuronal isolation and gene expression analysis in differentiated neurons.RNA sequencing technology is promising not only for the determination of gene expression,but also for discovery of posttranscriptional modiﬁcations of the complex neural system.There is no doubt that advances in genomic studies are opening up novel research avenues for our understanding of the cortical neuronal functions.

关键词： expression proﬁling pyramidal neurons RNA ampliﬁcation cortex retrograde labeling