{"title":"脑深部刺激诱导的两种消除帕金森病爆发的方式:突触电流和分叉机制。","authors":"Hui Zhou, Xianjun Wang, Huaguang Gu, Yanbing Jia","doi":"10.1007/s11571-025-10267-5","DOIUrl":null,"url":null,"abstract":"<p><p>Although deep brain stimulation (DBS) is effective in treating Parkinson's disease (PD) related to bursting, the underlying mechanisms remain unclear. In the present paper, the dynamical and synaptic mechanisms are studied in a basal ganglia-thalamus model. Firstly, slow and large oscillations of synaptic gating variables/currents are identified as the cause of the irregular and non-synchronous bursting for PD, indicating that interruption of these slow modulations may be a feasible measure to treat PD. Secondly, strong DBS with high frequency applied to subthalamic nucleus (STN) can induce fast synchronous spiking in both STN and external globus pallidus (GPe), then interrupt the slow gating variables, thereby eliminating the irregular bursting. Meanwhile, the gating variables of the excitatory and inhibitory synapses respectively from STN and GPe to the internal globus pallidus (GPi) become fast. Finally, competition between these two opposite synapses can induce two manners to eliminate the bursting of GPi and restore the normal state, appearing in vast majority of parameter space composed of multiple synaptic conductances. One is the synchronous silence of GPi, and the other the synchronous regular fast spiking, which occurs for large conductance of the inhibitory and excitatory synapse, respectively. Both result in regular spiking of thalamus, via interrupting slow gating variables of synapse projected to thalamus. In addition, as the two conductances approach each other, the synaptic current to GPi oscillates around zero slowly, resulting in irregular firings of GPi and thalamus for PD in a narrow parameter space. Furthermore, the bursting observed in PD before DBS and three types of electrical activities of GPi during DBS are explained, using a saddle-node bifurcation of limit cycles and oscillation patterns of synaptic current. The distinction from the post inhibitory rebound bursting reported in previous studies is discussed. The results present the mechanisms for DBS to treat PD via eliminating bursting in wide parameter region.</p>","PeriodicalId":10500,"journal":{"name":"Cognitive Neurodynamics","volume":"19 1","pages":"78"},"PeriodicalIF":3.1000,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12089561/pdf/","citationCount":"0","resultStr":"{\"title\":\"Deep brain stimulation-induced two manners to eliminate bursting for Parkinson's diseases: synaptic current and bifurcation mechanisms.\",\"authors\":\"Hui Zhou, Xianjun Wang, Huaguang Gu, Yanbing Jia\",\"doi\":\"10.1007/s11571-025-10267-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Although deep brain stimulation (DBS) is effective in treating Parkinson's disease (PD) related to bursting, the underlying mechanisms remain unclear. In the present paper, the dynamical and synaptic mechanisms are studied in a basal ganglia-thalamus model. Firstly, slow and large oscillations of synaptic gating variables/currents are identified as the cause of the irregular and non-synchronous bursting for PD, indicating that interruption of these slow modulations may be a feasible measure to treat PD. Secondly, strong DBS with high frequency applied to subthalamic nucleus (STN) can induce fast synchronous spiking in both STN and external globus pallidus (GPe), then interrupt the slow gating variables, thereby eliminating the irregular bursting. Meanwhile, the gating variables of the excitatory and inhibitory synapses respectively from STN and GPe to the internal globus pallidus (GPi) become fast. Finally, competition between these two opposite synapses can induce two manners to eliminate the bursting of GPi and restore the normal state, appearing in vast majority of parameter space composed of multiple synaptic conductances. One is the synchronous silence of GPi, and the other the synchronous regular fast spiking, which occurs for large conductance of the inhibitory and excitatory synapse, respectively. Both result in regular spiking of thalamus, via interrupting slow gating variables of synapse projected to thalamus. In addition, as the two conductances approach each other, the synaptic current to GPi oscillates around zero slowly, resulting in irregular firings of GPi and thalamus for PD in a narrow parameter space. Furthermore, the bursting observed in PD before DBS and three types of electrical activities of GPi during DBS are explained, using a saddle-node bifurcation of limit cycles and oscillation patterns of synaptic current. The distinction from the post inhibitory rebound bursting reported in previous studies is discussed. The results present the mechanisms for DBS to treat PD via eliminating bursting in wide parameter region.</p>\",\"PeriodicalId\":10500,\"journal\":{\"name\":\"Cognitive Neurodynamics\",\"volume\":\"19 1\",\"pages\":\"78\"},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2025-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12089561/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cognitive Neurodynamics\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.1007/s11571-025-10267-5\",\"RegionNum\":3,\"RegionCategory\":\"工程技术\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/5/19 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cognitive Neurodynamics","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1007/s11571-025-10267-5","RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/5/19 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Deep brain stimulation-induced two manners to eliminate bursting for Parkinson's diseases: synaptic current and bifurcation mechanisms.
Although deep brain stimulation (DBS) is effective in treating Parkinson's disease (PD) related to bursting, the underlying mechanisms remain unclear. In the present paper, the dynamical and synaptic mechanisms are studied in a basal ganglia-thalamus model. Firstly, slow and large oscillations of synaptic gating variables/currents are identified as the cause of the irregular and non-synchronous bursting for PD, indicating that interruption of these slow modulations may be a feasible measure to treat PD. Secondly, strong DBS with high frequency applied to subthalamic nucleus (STN) can induce fast synchronous spiking in both STN and external globus pallidus (GPe), then interrupt the slow gating variables, thereby eliminating the irregular bursting. Meanwhile, the gating variables of the excitatory and inhibitory synapses respectively from STN and GPe to the internal globus pallidus (GPi) become fast. Finally, competition between these two opposite synapses can induce two manners to eliminate the bursting of GPi and restore the normal state, appearing in vast majority of parameter space composed of multiple synaptic conductances. One is the synchronous silence of GPi, and the other the synchronous regular fast spiking, which occurs for large conductance of the inhibitory and excitatory synapse, respectively. Both result in regular spiking of thalamus, via interrupting slow gating variables of synapse projected to thalamus. In addition, as the two conductances approach each other, the synaptic current to GPi oscillates around zero slowly, resulting in irregular firings of GPi and thalamus for PD in a narrow parameter space. Furthermore, the bursting observed in PD before DBS and three types of electrical activities of GPi during DBS are explained, using a saddle-node bifurcation of limit cycles and oscillation patterns of synaptic current. The distinction from the post inhibitory rebound bursting reported in previous studies is discussed. The results present the mechanisms for DBS to treat PD via eliminating bursting in wide parameter region.
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.