Neuroscience bulletin最新文献_第9页

Sodium Leak Channel in Glutamatergic Neurons of the Lateral Parabrachial Nucleus Helps to Maintain Respiratory Frequency Under Sevoflurane Anesthesia. 副腋外侧核谷氨酸能神经元的钠漏通道有助于在七氟醚麻醉下维持呼吸频率

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2024-05-20 DOI: 10.1007/s12264-024-01223-0

Lin Wu, Donghang Zhang, Yujie Wu, Jin Liu, Jingyao Jiang, Cheng Zhou

{"title":"Sodium Leak Channel in Glutamatergic Neurons of the Lateral Parabrachial Nucleus Helps to Maintain Respiratory Frequency Under Sevoflurane Anesthesia.","authors":"Lin Wu, Donghang Zhang, Yujie Wu, Jin Liu, Jingyao Jiang, Cheng Zhou","doi":"10.1007/s12264-024-01223-0","DOIUrl":"10.1007/s12264-024-01223-0","url":null,"abstract":"The lateral parabrachial nucleus (PBL) is implicated in the regulation of respiratory activity. Sodium leak channel (NALCN) mutations disrupt the respiratory rhythm and influence anesthetic sensitivity in both rodents and humans. Here, we investigated whether the NALCN in PBL glutamatergic neurons maintains respiratory function under general anesthesia. Our results showed that chemogenetic activation of PBL glutamatergic neurons increased the respiratory frequency (RF) in mice; whereas chemogenetic inhibition suppressed RF. NALCN knockdown in PBL glutamatergic neurons but not GABAergic neurons significantly reduced RF under physiological conditions and caused more respiratory suppression under sevoflurane anesthesia. NALCN knockdown in PBL glutamatergic neurons did not further exacerbate the respiratory suppression induced by propofol or morphine. Under sevoflurane anesthesia, painful stimuli rapidly increased the RF, which was not affected by NALCN knockdown in PBL glutamatergic neurons. This study suggested that the NALCN is a key ion channel in PBL glutamatergic neurons that maintains respiratory frequency under volatile anesthetic sevoflurane but not intravenous anesthetic propofol.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"1127-1140"},"PeriodicalIF":5.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141066114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Abnormal Innervation, Demyelination, and Degeneration of Spiral Ganglion Neurons as Well as Disruption of Heminodes are Involved in the Onset of Deafness in Cx26 Null Mice. Cx26缺失小鼠耳聋的发生与螺旋神经节神经元的异常神经支配、脱髓鞘和变性以及半结节的破坏有关。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2024-02-04 DOI: 10.1007/s12264-023-01167-x

Yue Qiu, Le Xie, Xiaohui Wang, Kai Xu, Xue Bai, Sen Chen, Yu Sun

{"title":"Abnormal Innervation, Demyelination, and Degeneration of Spiral Ganglion Neurons as Well as Disruption of Heminodes are Involved in the Onset of Deafness in Cx26 Null Mice.","authors":"Yue Qiu, Le Xie, Xiaohui Wang, Kai Xu, Xue Bai, Sen Chen, Yu Sun","doi":"10.1007/s12264-023-01167-x","DOIUrl":"10.1007/s12264-023-01167-x","url":null,"abstract":"GJB2 gene mutations are the most common causes of autosomal recessive non-syndromic hereditary deafness. For individuals suffering from severe to profound GJB2-related deafness, cochlear implants have emerged as the sole remedy for auditory improvement. Some previous studies have highlighted the crucial role of preserving cochlear neural components in achieving favorable outcomes after cochlear implantation. Thus, we generated a conditional knockout mouse model (Cx26-CKO) in which Cx26 was completely deleted in the cochlear supporting cells driven by the Sox2 promoter. The Cx26-CKO mice showed severe hearing loss and massive loss of hair cells and Deiter's cells, which represented the extreme form of human deafness caused by GJB2 gene mutations. In addition, multiple pathological changes in the peripheral auditory nervous system were found, including abnormal innervation, demyelination, and degeneration of spiral ganglion neurons as well as disruption of heminodes in Cx26-CKO mice. These findings provide invaluable insights into the deafness mechanism and the treatment for severe deafness in Cx26-null mice.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"1093-1103"},"PeriodicalIF":5.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139681249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dopamine Switches Affective States Under Acute Sleep Deprivation. 多巴胺能切换急性睡眠剥夺状态下的情感状态

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2024-05-09 DOI: 10.1007/s12264-024-01216-z

Zhou-Cai Luo, Tian-Ming Gao

引用次数: 0

Aβ-Aggregation-Generated Blue Autofluorescence Illuminates Senile Plaques as well as Complex Blood and Vascular Pathologies in Alzheimer's Disease. Aβ聚集产生的蓝色自发荧光可照亮老年痴呆症的老年斑以及复杂的血液和血管病变。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2024-02-12 DOI: 10.1007/s12264-023-01175-x

Hualin Fu, Jilong Li, Chunlei Zhang, Peng Du, Guo Gao, Qiqi Ge, Xinping Guan, Daxiang Cui

{"title":"Aβ-Aggregation-Generated Blue Autofluorescence Illuminates Senile Plaques as well as Complex Blood and Vascular Pathologies in Alzheimer's Disease.","authors":"Hualin Fu, Jilong Li, Chunlei Zhang, Peng Du, Guo Gao, Qiqi Ge, Xinping Guan, Daxiang Cui","doi":"10.1007/s12264-023-01175-x","DOIUrl":"10.1007/s12264-023-01175-x","url":null,"abstract":"Senile plaque blue autofluorescence was discovered around 40 years ago, however, its impact on Alzheimer's disease (AD) pathology has not been fully examined. We analyzed senile plaques with immunohistochemistry and fluorescence imaging on AD brain sections and also Aβ aggregation in vitro. In DAPI or Hoechst staining, the nuclear blue fluorescence could only be correctly assigned after subtracting the blue plaque autofluorescence. The flower-like structures wrapping dense-core blue fluorescence formed by cathepsin D staining could not be considered central-nucleated neurons with defective lysosomes since there was no nuclear staining in the plaque core when the blue autofluorescence was subtracted. Both Aβ self-oligomers and Aβ/hemoglobin heterocomplexes generated blue autofluorescence. The Aβ amyloid blue autofluorescence not only labels senile plaques but also illustrates red cell aggregation, hemolysis, cerebral amyloid angiopathy, vascular plaques, vascular adhesions, and microaneurysms. In summary, we conclude that Aβ-aggregation-generated blue autofluorescence is an excellent multi-amyloidosis marker in Alzheimer's disease.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"1115-1126"},"PeriodicalIF":5.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306447/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139723426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Serum LDL Promotes Microglial Activation and Exacerbates Demyelinating Injury in Neuromyelitis Optica Spectrum Disorder. 血清低密度脂蛋白促进小胶质细胞活化并加剧神经脊髓炎谱系障碍的脱髓鞘损伤

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2024-01-16 DOI: 10.1007/s12264-023-01166-y

Man Chen, Yun-Hui Chu, Wen-Xiang Yu, Yun-Fan You, Yue Tang, Xiao-Wei Pang, Hang Zhang, Ke Shang, Gang Deng, Luo-Qi Zhou, Sheng Yang, Wei Wang, Jun Xiao, Dai-Shi Tian, Chuan Qin

{"title":"Serum LDL Promotes Microglial Activation and Exacerbates Demyelinating Injury in Neuromyelitis Optica Spectrum Disorder.","authors":"Man Chen, Yun-Hui Chu, Wen-Xiang Yu, Yun-Fan You, Yue Tang, Xiao-Wei Pang, Hang Zhang, Ke Shang, Gang Deng, Luo-Qi Zhou, Sheng Yang, Wei Wang, Jun Xiao, Dai-Shi Tian, Chuan Qin","doi":"10.1007/s12264-023-01166-y","DOIUrl":"10.1007/s12264-023-01166-y","url":null,"abstract":"Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory demyelinating disease of the central nervous system (CNS) accompanied by blood-brain barrier (BBB) disruption. Dysfunction in microglial lipid metabolism is believed to be closely associated with the neuropathology of NMOSD. However, there is limited evidence on the functional relevance of circulating lipids in CNS demyelination, cellular metabolism, and microglial function. Here, we found that serum low-density lipoprotein (LDL) was positively correlated with markers of neurological damage in NMOSD patients. In addition, we demonstrated in a mouse model of NMOSD that LDL penetrates the CNS through the leaky BBB, directly activating microglia. This activation leads to excessive phagocytosis of myelin debris, inhibition of lipid metabolism, and increased glycolysis, ultimately exacerbating myelin damage. We also found that therapeutic interventions aimed at reducing circulating LDL effectively reversed the lipid metabolic dysfunction in microglia and mitigated the demyelinating injury in NMOSD. These findings shed light on the molecular and cellular mechanisms underlying the positive correlation between serum LDL and neurological damage, highlighting the potential therapeutic target for lowering circulating lipids to alleviate the acute demyelinating injury in NMOSD.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"1104-1114"},"PeriodicalIF":5.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139472803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epitranscriptomic Regulation of NMDA Receptors Rears its Ugly Head in Chemotherapy-Induced Neuropathic Pain. 化疗诱发的神经病理性疼痛中 NMDA 受体的外转录组调控显露狰狞面目

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2024-05-08 DOI: 10.1007/s12264-024-01220-3

Wing Lam Yu, Gerald W Zamponi

引用次数: 0

Closing the Experiment-Modeling-Perturbation Loop in Whole-Brain Neuroscience. 关闭全脑神经科学中的实验-建模-扰动回路

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2024-07-16 DOI: 10.1007/s12264-024-01253-8

Misha B Ahrens

引用次数: 0

Fluoxetine Rescues Excessive Myelin Formation and Psychological Behaviors in a Murine PTSD Model. 氟西汀能挽救创伤后应激障碍小鼠模型中的过度髓鞘形成和心理行为

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2024-07-16 DOI: 10.1007/s12264-024-01249-4

Chenrui Yin, Kefei Luo, Xinyue Zhu, Ronghang Zheng, Yu Wang, Guangdan Yu, Xiaorui Wang, Fei She, Xiaoying Chen, Tao Li, Jingfei Chen, Baduojie Bian, Yixun Su, Jianqin Niu, Yuxin Wang

{"title":"Fluoxetine Rescues Excessive Myelin Formation and Psychological Behaviors in a Murine PTSD Model.","authors":"Chenrui Yin, Kefei Luo, Xinyue Zhu, Ronghang Zheng, Yu Wang, Guangdan Yu, Xiaorui Wang, Fei She, Xiaoying Chen, Tao Li, Jingfei Chen, Baduojie Bian, Yixun Su, Jianqin Niu, Yuxin Wang","doi":"10.1007/s12264-024-01249-4","DOIUrl":"10.1007/s12264-024-01249-4","url":null,"abstract":"Posttraumatic stress disorder (PTSD) is a complex mental disorder notable for traumatic experience memory. Although current first-line treatments are linked with clinically important symptom reduction, a large proportion of patients retained to experience considerable residual symptoms, indicating pathogenic mechanism should be illustrated further. Recent studies reported that newly formed myelin could shape neural circuit function and be implicated in fear memory preservation. However, its role in PTSD remains to be elucidated. In this study, we adopted a restraint stress-induced PTSD mouse model and found that PTSD-related neuropsychiatric symptoms were accompanied by increased myelination in the posterior parietal cortex and hippocampus. Fluoxetine, but not risperidone or sertraline, has a more profound rescue effect on neuropsychological behaviors and myelin abnormalities. Further mechanistic experiments revealed that fluoxetine could directly interfere with oligodendroglial differentiation by upregulating Wnt signaling. Our data demonstrated the correlation between PTSD and abnormal myelination, suggesting that the oligodendroglial lineage could be a target for PTSD treatment.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"1037-1052"},"PeriodicalIF":5.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Myosin Va-dependent Transport of NMDA Receptors in Hippocampal Neurons. 海马神经元中 NMDA 受体的肌球蛋白 Va 依赖性运输

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2024-01-30 DOI: 10.1007/s12264-023-01174-y

Ru Gong, Linwei Qin, Linlin Chen, Ning Wang, Yifei Bao, Wei Lu

引用次数: 0

TRP Channels in Stroke. 行程中的TRP通道。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2024-08-01 Epub Date: 2023-11-23 DOI: 10.1007/s12264-023-01151-5

Pengyu Zong, Cindy X Li, Jianlin Feng, Mara Cicchetti, Lixia Yue

引用次数: 0