{"title":"调节人体 L2/3 锥体神经元的 XOR 功能","authors":"Yanheng Li, Ruiming Zhang, Xiaojuan Sun","doi":"10.1007/s11571-024-10175-0","DOIUrl":null,"url":null,"abstract":"<p>The apical dendrites of human L2/3 pyramidal neurons are capable of performing XOR computation by modulating the amplitude of dendritic calcium action potentials (dCaAPs) mediated by calcium ions. What influences this particular function? There is still no answer to this question. In this study, we employed a rational and feasible reduction method to successfully derive simplified models of human L2/3 pyramidal neurons while preserving their detailed functional properties. Using a conductance-based model, we manipulated the membrane potential of the apical dendrite in the simplified model. Our findings indicate that an increase in sodium conductance (<span>\\({g}_{Na}\\)</span>) and membrane capacitance (<span>\\({C}_{m}\\)</span>) weakens the XOR function, while regulation of potassium conductance (<span>\\({g}_{K}\\)</span>) demonstrates robustness in maintaining the XOR function. Further analysis reveals that when a single pathway is activated, an increase in <span>\\({g}_{Na}\\)</span> and <span>\\({C}_{m}\\)</span> leads to decrease in the amplitude of dCaAPs, whereas increasing <span>\\({g}_{K}\\)</span> has a relatively minor impact on dCaAPs amplitude. In conclusion, although calcium ions play a crucial role in enabling apical dendrites of human L2/3 pyramidal neurons to perform XOR computation, other ion channels’ conductance and membrane capacitance can also influence this function.</p>","PeriodicalId":10500,"journal":{"name":"Cognitive Neurodynamics","volume":null,"pages":null},"PeriodicalIF":3.1000,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Regulation of XOR function of reduced human L2/3 pyramidal neurons\",\"authors\":\"Yanheng Li, Ruiming Zhang, Xiaojuan Sun\",\"doi\":\"10.1007/s11571-024-10175-0\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>The apical dendrites of human L2/3 pyramidal neurons are capable of performing XOR computation by modulating the amplitude of dendritic calcium action potentials (dCaAPs) mediated by calcium ions. What influences this particular function? There is still no answer to this question. In this study, we employed a rational and feasible reduction method to successfully derive simplified models of human L2/3 pyramidal neurons while preserving their detailed functional properties. Using a conductance-based model, we manipulated the membrane potential of the apical dendrite in the simplified model. Our findings indicate that an increase in sodium conductance (<span>\\\\({g}_{Na}\\\\)</span>) and membrane capacitance (<span>\\\\({C}_{m}\\\\)</span>) weakens the XOR function, while regulation of potassium conductance (<span>\\\\({g}_{K}\\\\)</span>) demonstrates robustness in maintaining the XOR function. Further analysis reveals that when a single pathway is activated, an increase in <span>\\\\({g}_{Na}\\\\)</span> and <span>\\\\({C}_{m}\\\\)</span> leads to decrease in the amplitude of dCaAPs, whereas increasing <span>\\\\({g}_{K}\\\\)</span> has a relatively minor impact on dCaAPs amplitude. In conclusion, although calcium ions play a crucial role in enabling apical dendrites of human L2/3 pyramidal neurons to perform XOR computation, other ion channels’ conductance and membrane capacitance can also influence this function.</p>\",\"PeriodicalId\":10500,\"journal\":{\"name\":\"Cognitive Neurodynamics\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2024-09-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cognitive Neurodynamics\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.1007/s11571-024-10175-0\",\"RegionNum\":3,\"RegionCategory\":\"工程技术\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cognitive Neurodynamics","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1007/s11571-024-10175-0","RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Regulation of XOR function of reduced human L2/3 pyramidal neurons
The apical dendrites of human L2/3 pyramidal neurons are capable of performing XOR computation by modulating the amplitude of dendritic calcium action potentials (dCaAPs) mediated by calcium ions. What influences this particular function? There is still no answer to this question. In this study, we employed a rational and feasible reduction method to successfully derive simplified models of human L2/3 pyramidal neurons while preserving their detailed functional properties. Using a conductance-based model, we manipulated the membrane potential of the apical dendrite in the simplified model. Our findings indicate that an increase in sodium conductance (\({g}_{Na}\)) and membrane capacitance (\({C}_{m}\)) weakens the XOR function, while regulation of potassium conductance (\({g}_{K}\)) demonstrates robustness in maintaining the XOR function. Further analysis reveals that when a single pathway is activated, an increase in \({g}_{Na}\) and \({C}_{m}\) leads to decrease in the amplitude of dCaAPs, whereas increasing \({g}_{K}\) has a relatively minor impact on dCaAPs amplitude. In conclusion, although calcium ions play a crucial role in enabling apical dendrites of human L2/3 pyramidal neurons to perform XOR computation, other ion channels’ conductance and membrane capacitance can also influence this function.
期刊介绍:
Cognitive Neurodynamics provides a unique forum of communication and cooperation for scientists and engineers working in the field of cognitive neurodynamics, intelligent science and applications, bridging the gap between theory and application, without any preference for pure theoretical, experimental or computational models.
The emphasis is to publish original models of cognitive neurodynamics, novel computational theories and experimental results. In particular, intelligent science inspired by cognitive neuroscience and neurodynamics is also very welcome.
The scope of Cognitive Neurodynamics covers cognitive neuroscience, neural computation based on dynamics, computer science, intelligent science as well as their interdisciplinary applications in the natural and engineering sciences. Papers that are appropriate for non-specialist readers are encouraged.
1. There is no page limit for manuscripts submitted to Cognitive Neurodynamics. Research papers should clearly represent an important advance of especially broad interest to researchers and technologists in neuroscience, biophysics, BCI, neural computer and intelligent robotics.
2. Cognitive Neurodynamics also welcomes brief communications: short papers reporting results that are of genuinely broad interest but that for one reason and another do not make a sufficiently complete story to justify a full article publication. Brief Communications should consist of approximately four manuscript pages.
3. Cognitive Neurodynamics publishes review articles in which a specific field is reviewed through an exhaustive literature survey. There are no restrictions on the number of pages. Review articles are usually invited, but submitted reviews will also be considered.