Cognitive Neurodynamics

, Volume 9, Issue 3, pp 279–289 | Cite as

Control of absence seizures induced by the pathways connected to SRN in corticothalamic system

  • Bing Hu
  • Daqing Guo
  • Qingyun WangEmail author
Research Article


The cerebral cortex, thalamus and basal ganglia together form an important network in the brain, which is closely related to several nerve diseases, such as parkinson disease, epilepsy seizure and so on. Absence seizure can be characterized by 2–4 Hz oscillatory activity, and it can be induced by abnormal interactions between the cerebral cortex and thalamus. Many experimental results have also shown that basal ganglia are a key neural structure, which closely links the corticothalamic system in the brain. Presently, we use a corticothalamic-basal ganglia model to study which pathways in corticothalamic system can induce absence seizures and how these oscillatory activities can be controlled by projections from the substantia nigra pars reticulata (SNr) to the thalamic reticular nucleus (TRN) or the specific relay nuclei (SRN) of the thalamus. By tuning the projection strength of the pathway “Excitatory pyramidal cortex-SRN”, ”SRN-Excitatory pyramidal cortex” and “SRN–TRN” respectively, different firing states including absence seizures can appear. This indicates that absence seizures can be induced by tuning the connection strength of the considered pathway. In addition, typical absence epilepsy seizure state “spike-and-slow wave discharges” can be controlled by adjusting the activation level of the SNr as the pathways SNr–SRN and SNr–TRN open independently or together. Our results emphasize the importance of basal ganglia in controlling absence seizures in the corticothalamic system, and can provide a potential idea for the clinical treatment.


Basal ganglia Absence seizures Control 



This research was supported by the National Science Foundation of China (Grant Nos. 11325208, 11172017 and 61201278).


  1. Biraben A, Semah F et al (2004) PET evidence for a role of the basal ganglia in patients with ring chromosome 20 epilepsy. Neurology 63:73–77CrossRefPubMedGoogle Scholar
  2. Breakspear M, Roberts JA et al (2006) A unifying explanation of primary generalized seizures through nonlinear brain modeling and bifurcation analysis. Cereb Cortex 16:1296–1313CrossRefPubMedGoogle Scholar
  3. Chen MM, Guo DQ et al (2014) Bidirectional control of absence seizures by the Basal Ganglia: a computational evidence. PLoS Comput Biol 10(3):e1003495CrossRefPubMedCentralPubMedGoogle Scholar
  4. Coenen AM, van Luijtelaar EL (2003) Genetic animal models for absence epilepsy: a review of the WAG/Rij strain of rats. Behav Genet 33:635–655CrossRefPubMedGoogle Scholar
  5. Crunelli V, Leresche N (2002) Childhood absence epilepsy: genes, channels, neurons and networks. Nat Rev Neurosci 3:371–382CrossRefPubMedGoogle Scholar
  6. Deransart C, Depaulis A (2002) The control of seizures by the basal ganglia? A review of experimental data. Epileptic Disord Suppl 3:S61–72Google Scholar
  7. Deransart C, Vercueil L et al (1998) The role of basal ganglia in the control of generalized absence seizures. Epilepsy Res 32:213–223CrossRefPubMedGoogle Scholar
  8. Gatev P, Wichmann T (2008) Interactions between cortical rhythms and spiking activity of single basal ganglia neurons in the normal and parkinsonian state. Cereb Cortex 19(6):1330–1344CrossRefPubMedCentralPubMedGoogle Scholar
  9. Groenewegen HJ (2003) The basal ganglia and motor control. Neural Plast 10:107–120CrossRefPubMedCentralPubMedGoogle Scholar
  10. Gulcebi MI, Ketenci S et al (2012) Topographical connections of the substantia nigra pars reticulata to higher-order thalamic nuclei in the rat. Brain Res Bull 87:312–318CrossRefPubMedGoogle Scholar
  11. Humphries MD, Gurney K (2012) Network effects of subthalamic deep brain stimulation drive a unique mixture of responses in basal ganglia output. Eur J Neurosci 36:2240–2251CrossRefPubMedGoogle Scholar
  12. Jasper HH, Kershman J (1941) Electroencephalographic classification of the epilepsies. Arch Neurol Psychiatry 45:903–943CrossRefGoogle Scholar
  13. Kase D, Inoue T et al (2012) Roles of the subthalamic nucleus and subthalamic HCN channels in absence seizures. J Neurophysiol 107:393–406CrossRefPubMedGoogle Scholar
  14. Marten F, Rodrigues S et al (2009) Onset of polyspike complexes in a mean-field model of human electroencephalography and its application to absence epilepsy. Phil Trans R Soc A 367:1145–1161CrossRefPubMedGoogle Scholar
  15. Massimo A (2012) A brief history on the oscillating roles of thalamus and cortex in absence seizures. Epilepsia 53(5):779–789CrossRefGoogle Scholar
  16. Park C, Rubchinsky LL (2012) Potential Mechanisms for Imperfect Synchronization in Parkinsonian basal Ggnglia. PLOS ONE 7(12):e51530CrossRefPubMedCentralPubMedGoogle Scholar
  17. Paz JT, Bryant AS et al (2011) A new mode of corticothalamic transmission revealed in the \(Gria4^{-/-}\) model of absence epilepsy. Nat Neurosci 14(9):1167–1173CrossRefPubMedCentralPubMedGoogle Scholar
  18. Paz JT, Chavez M et al (2007) Activity of ventral medial thalamic neurons during absence seizures and modulation of cortical paroxysms by the nigrothalamic pathway. J Neurosci 27:929–941CrossRefPubMedGoogle Scholar
  19. Paz JT, Deniau JM et al (2005) Rhythmic bursting in the cortico-subthalamo-pallidal network during spontaneous genetically determined spike and wave discharges. J Neurosci 25(8):2092–2101CrossRefPubMedGoogle Scholar
  20. Roberts JA, Robinson PA (2008) Modeling absence seizure dynamics: implications for basic mechanisms and measurement of thalamocortical and corticothalamic latencies. J Theor Biol 253:189–201CrossRefPubMedGoogle Scholar
  21. Robinson PA, Rennie CJ et al (1998) Steady states and global dynamics of electrical activity in the cerebral cortex. Phys Rev E 58:3557–3571CrossRefGoogle Scholar
  22. Robinson PA, Rennie CJ et al (2001) Prediction of electroencephalographic spectra from neurophysiology. Phys Rev E 63:021903CrossRefGoogle Scholar
  23. Robinson PA, Rennie CJ et al (2002) Dynamics of large-scale brain activity in normal arousal states and epileptic seizures. Phys Rev E 65:041924CrossRefGoogle Scholar
  24. Robinson PA, Rennie CJ et al (2003) Estimation of multiscale neurophysiologic parameters by electroencephalographic means. Hum Brain Mapp 23:53–72CrossRefGoogle Scholar
  25. Rodrigues S, Barton D et al (2009) Transitions to spike-wave oscillations and epileptic dynamics in a human cortico-thalamic mean-field model. J Comput Neurosci 27(3):507–526CrossRefPubMedGoogle Scholar
  26. Timofeev I, Steriade M (2004) Neocortical seizures: initiation, development and cessation. Neuroscience 123:299–336CrossRefPubMedGoogle Scholar
  27. van Albada SJ, Gray RT et al (2009) Mean-field modeling of the basal ganglia-thalamocortical system. II: dynamics of parkinsonian oscillations. J Theor Biol 257:664–688CrossRefPubMedGoogle Scholar
  28. van Albada SJ, Robinson PA (2009) Mean-field modeling of the basal ganglia-thalamocortical system. I: firing rates in healthy and parkinsonian states. J Theor Biol 257:642–663CrossRefPubMedGoogle Scholar
  29. van Luijtelaar G, Sitnikova E (2006) Global and focal aspects of absence epilepsy: the contribution of genetic models. Neurosci Biobehav Rev 30:983–1003CrossRefPubMedGoogle Scholar
  30. Volman V, Perc M, Bazhenov M (2011) Gap junctions and epileptic seizures: two sides of the same coin? PLoS One 6(5):e20572CrossRefPubMedCentralPubMedGoogle Scholar

Copyright information

© Springer Science+Business Media Dordrecht 2014

Authors and Affiliations

  1. 1.Department of Dynamics and ControlBeihang UniversityBeijingChina
  2. 2.Key Laboratory for Neuro Information of Ministry of Education, School of Life Science and TechnologyUniversity of Electronic Science and Technology of ChinaChengduChina

Personalised recommendations