{"title":"Accurate Machine Learning-based Monitoring of Anesthesia Depth with EEG Recording","authors":"Zhiyi Tu, Yuehan Zhang, Xueyang Lv, Yanyan Wang, Tingting Zhang, Juan Wang, Xinren Yu, Pei Chen, Suocheng Pang, Shengtian Li, Xiongjie Yu, Xuan Zhao","doi":"10.1007/s12264-024-01297-w","DOIUrl":"https://doi.org/10.1007/s12264-024-01297-w","url":null,"abstract":"<p>General anesthesia, pivotal for surgical procedures, requires precise depth monitoring to mitigate risks ranging from intraoperative awareness to postoperative cognitive impairments. Traditional assessment methods, relying on physiological indicators or behavioral responses, fall short of accurately capturing the nuanced states of unconsciousness. This study introduces a machine learning-based approach to decode anesthesia depth, leveraging EEG data across different anesthesia states induced by propofol and esketamine in rats. Our findings demonstrate the model’s robust predictive accuracy, underscored by a novel intra-subject dataset partitioning and a 5-fold cross-validation method. The research diverges from conventional monitoring by utilizing anesthetic infusion rates as objective indicators of anesthesia states, highlighting distinct EEG patterns and enhancing prediction accuracy. Moreover, the model’s ability to generalize across individuals suggests its potential for broad clinical application, distinguishing between anesthetic agents and their depths. Despite relying on rat EEG data, which poses questions about real-world applicability, our approach marks a significant advance in anesthesia monitoring.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":"57 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"GABAergic Retinal Ganglion Cells Projecting to the Superior Colliculus Mediate the Looming-Evoked Flight Response","authors":"Man Yuan, Gao Tan, Danrui Cai, Xue Luo, Kejiong Shen, Qinqin Deng, Xinlan Lei, Wen-Bo Zeng, Min-Hua Luo, Lu Huang, Chaoran Ren, Yin Shen","doi":"10.1007/s12264-024-01295-y","DOIUrl":"https://doi.org/10.1007/s12264-024-01295-y","url":null,"abstract":"<p>The looming stimulus-evoked flight response to approaching predators is a defensive behavior in most animals. However, how looming stimuli are detected in the retina and transmitted to the brain remains unclear. Here, we report that a group of GABAergic retinal ganglion cells (RGCs) projecting to the superior colliculus (SC) transmit looming signals from the retina to the brain, mediating the looming-evoked flight behavior by releasing GABA. <i>GAD2-Cre</i> and <i>vGAT-Cre</i> transgenic mice were used in combination with Cre-activated anterograde or retrograde tracer viruses to map the inputs to specific GABAergic RGC circuits. Optogenetic technology was used to assess the function of SC-projecting GABAergic RGCs (scpgRGCs) in the SC. FDIO-DTA (Flp-dependent Double-Floxed Inverted Open reading frame-Diphtheria toxin) combined with the FLP (Florfenicol, Lincomycin & Prednisolone) approach was used to ablate or silence scpgRGCs. In the mouse retina, GABAergic RGCs project to different brain areas, including the SC. ScpgRGCs are monosynaptically connected to parvalbumin-positive SC neurons known to be required for the looming-evoked flight response. Optogenetic activation of scpgRGCs triggers GABA-mediated inhibition in SC neurons. Ablation or silencing of scpgRGCs compromises looming-evoked flight responses without affecting image-forming functions. Our study reveals that scpgRGCs control the looming-evoked flight response by regulating SC neurons via GABA, providing novel insight into the regulation of innate defensive behaviors.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":"50 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hong Chen, Gang Yang, De-En Xu, Yu-tong Du, Chao Zhu, Hua Hu, Li Luo, Lei Feng, Wenhui Huang, Yan-Yun Sun, Quan-Hong Ma
{"title":"Autophagy in Oligodendrocyte Lineage Cells Controls Oligodendrocyte Numbers and Myelin Integrity in an Age-dependent Manner","authors":"Hong Chen, Gang Yang, De-En Xu, Yu-tong Du, Chao Zhu, Hua Hu, Li Luo, Lei Feng, Wenhui Huang, Yan-Yun Sun, Quan-Hong Ma","doi":"10.1007/s12264-024-01292-1","DOIUrl":"https://doi.org/10.1007/s12264-024-01292-1","url":null,"abstract":"<p>Oligodendrocyte lineage cells, including oligodendrocyte precursor cells (OPCs) and oligodendrocytes (OLs), are essential in establishing and maintaining brain circuits. Autophagy is a conserved process that keeps the quality of organelles and proteostasis. The role of autophagy in oligodendrocyte lineage cells remains unclear. The present study shows that autophagy is required to maintain the number of OPCs/OLs and myelin integrity during brain aging. Inactivation of autophagy in oligodendrocyte lineage cells increases the number of OPCs/OLs in the developing brain while exaggerating the loss of OPCs/OLs with brain aging. Inactivation of autophagy in oligodendrocyte lineage cells impairs the turnover of myelin basic protein (MBP). It causes MBP to accumulate in the cytoplasm as multimeric aggregates and fails to be incorporated into integral myelin, which is associated with attenuated endocytic recycling. Inactivation of autophagy in oligodendrocyte lineage cells impairs myelin integrity and causes demyelination. Thus, this study shows autophagy is required to maintain myelin quality during aging by controlling the turnover of myelin components.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":"34 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Melatonin Ameliorates Abnormal Sleep-Wake Behavior via Facilitating Lipid Metabolism in a Zebrafish Model of Parkinson’s Disease","authors":"Meng-Zhu Pang, Han-Xing Li, Xue-Qin Dai, Xiao-Bo Wang, Jun-Yi Liu, Yun Shen, Xing Xu, Zhao-Min Zhong, Han Wang, Chun-Feng Liu, Fen Wang","doi":"10.1007/s12264-024-01299-8","DOIUrl":"https://doi.org/10.1007/s12264-024-01299-8","url":null,"abstract":"<p>Sleep-wake disorder is one of the most common nonmotor symptoms of Parkinson's disease (PD). Melatonin has the potential to improve sleep-wake disorder, but its mechanism of action is still unclear. Our data showed that melatonin only improved the motor and sleep-wake behavior of a zebrafish PD model when melatonin receptor 1 was present. Thus, we explored the underlying mechanisms by applying a rotenone model. After the PD zebrafish model was induced by 10 nmol/L rotenone, the motor and sleep-wake behavior were assessed. <i>In situ</i> hybridization and real-time quantitative PCR were used to detect the expression of melatonin receptors and lipid-metabolism-related genes. In the PD model, we found abnormal lipid metabolism, which was reversed by melatonin. This may be one of the main pathways for improving PD sleep-wake disorder.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":"41 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Spatiotemporal Mapping of the Oxytocin Receptor at Single-Cell Resolution in the Postnatally Developing Mouse Brain","authors":"Hao Li, Ying Li, Ting Wang, Shen Li, Heli Liu, Shuyi Ning, Wei Shen, Zhe Zhao, Haitao Wu","doi":"10.1007/s12264-024-01296-x","DOIUrl":"https://doi.org/10.1007/s12264-024-01296-x","url":null,"abstract":"<p>The oxytocin receptor (OXTR) has garnered increasing attention for its role in regulating both mature behaviors and brain development. It has been established that OXTR mediates a range of effects that are region-specific or period-specific. However, the current studies of OXTR expression patterns in mice only provide limited help due to limitations in resolution. Therefore, our objective was to generate a comprehensive, high-resolution spatiotemporal expression map of <i>Oxtr</i> mRNA across the entire developing mouse brain. We applied RNAscope <i>in situ</i> hybridization to investigate the spatiotemporal expression pattern of <i>Oxtr</i> in the brains of male mice at six distinct postnatal developmental stages (P7, P14, P21, P28, P42, P56). We provide detailed descriptions of <i>Oxtr</i> expression patterns in key brain regions, including the cortex, basal forebrain, hippocampus, and amygdaloid complex, with a focus on the precise localization of <i>Oxtr</i><sup>+</sup> cells and the variance of expression between different neurons. Furthermore, we identified some neuronal populations with high <i>Oxtr</i> expression levels that have been little studied, including glutamatergic neurons in the ventral dentate gyrus, <i>Vgat</i><sup>+</sup><i>Oxtr</i><sup>+</sup> cells in the basal forebrain, and GABAergic neurons in layers 4/5 of the cortex. Our study provides a novel perspective for understanding the distribution of <i>Oxtr</i> and encourages further investigations into its functions.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":"222 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ksenia Skobeleva, Guanghui Wang, Elena Kaznacheyeva
{"title":"STIM Proteins: The Gas and Brake of Calcium Entry in Neurons","authors":"Ksenia Skobeleva, Guanghui Wang, Elena Kaznacheyeva","doi":"10.1007/s12264-024-01272-5","DOIUrl":"https://doi.org/10.1007/s12264-024-01272-5","url":null,"abstract":"<p>Stromal interaction molecules (STIM)s are Ca<sup>2+</sup> sensors in internal Ca<sup>2+</sup> stores of the endoplasmic reticulum. They activate the store-operated Ca<sup>2+</sup> channels, which are the main source of Ca<sup>2+</sup> entry in non-excitable cells. Moreover, STIM proteins interact with other Ca<sup>2+</sup> channel subunits and active transporters, making STIMs an important intermediate molecule in orchestrating a wide variety of Ca<sup>2+</sup> influxes into excitable cells. Nevertheless, little is known about the role of STIM proteins in brain functioning. Being involved in many signaling pathways, STIMs replenish internal Ca<sup>2+</sup> stores in neurons and mediate synaptic transmission and neuronal excitability. Ca<sup>2+</sup> dyshomeostasis is a signature of many pathological conditions of the brain, including neurodegenerative diseases, injuries, stroke, and epilepsy. STIMs play a role in these disturbances not only by supporting abnormal store-operated Ca<sup>2+</sup> entry but also by regulating Ca<sup>2+</sup> influx through other channels. Here, we review the present knowledge of STIMs in neurons and their involvement in brain pathology.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":"81 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142178789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaonan Guo, Lizichen Chen, Jianbo Lai, Shaohua Hu
{"title":"Constructing A Theoretical Model to Bridge Neural Transition with a State Switch in Bipolar Disorder","authors":"Xiaonan Guo, Lizichen Chen, Jianbo Lai, Shaohua Hu","doi":"10.1007/s12264-024-01298-9","DOIUrl":"https://doi.org/10.1007/s12264-024-01298-9","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":"144 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142178790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shihao Huang, Xiaoxing Liu, Zhonghao Li, Yue Si, Liping Yang, Jiahui Deng, Yixiao Luo, Yan-Xue Xue, Lin Lu
{"title":"Memory Reconsolidation Updating in Substance Addiction: Applications, Mechanisms, and Future Prospects for Clinical Therapeutics","authors":"Shihao Huang, Xiaoxing Liu, Zhonghao Li, Yue Si, Liping Yang, Jiahui Deng, Yixiao Luo, Yan-Xue Xue, Lin Lu","doi":"10.1007/s12264-024-01294-z","DOIUrl":"https://doi.org/10.1007/s12264-024-01294-z","url":null,"abstract":"<p>Persistent and maladaptive drug-related memories represent a key component in drug addiction. Converging evidence from both preclinical and clinical studies has demonstrated the potential efficacy of the memory reconsolidation updating procedure (MRUP), a non-pharmacological strategy intertwining two distinct memory processes: reconsolidation and extinction—alternatively termed “the memory retrieval-extinction procedure”. This procedure presents a promising approach to attenuate, if not erase, entrenched drug memories and prevent relapse. The present review delineates the applications, molecular underpinnings, and operational boundaries of MRUP in the context of various forms of substance dependence. Furthermore, we critically examine the methodological limitations of MRUP, postulating potential refinement to optimize its therapeutic efficacy. In addition, we also look at the potential integration of MRUP and neurostimulation treatments in the domain of substance addiction. Overall, existing studies underscore the significant potential of MRUP, suggesting that interventions predicated on it could herald a promising avenue to enhance clinical outcomes in substance addiction therapy.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":"2016 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142178791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}