% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@INPROCEEDINGS{Bahuguna:829370,
      author       = {Bahuguna, Jyotika and Tetzlaff, Tom and Arvind, Kumar and
                      Kotaleski, Jeanette Hellgren and Morrison, Abigail},
      title        = {{H}omologous basal-ganglia networks in physiological and
                      parkinsonian conditions},
      reportid     = {FZJ-2017-03085},
      year         = {2017},
      abstract     = {The classical model of basal ganglia (BG) has been
                      regularly updated with discoveries of new sub-populations
                      within a nucleus or new projections from existing nuclei in
                      recent years. It is unclear how these new insights on the
                      structure of the BG network foster our understanding of its
                      function. The effective connectivities among these recently
                      identified BG sub-populations are only partially known. In
                      the framework of a simple firing-rate model subjected to a
                      genetic algorithm, we identified effective BG connectivities
                      which are consistent with experimentally established
                      firing-rate and phase relationships in Subthalamic Nucleus
                      (STN) and two GPe subpopulations (arkypallidal [GPe-TA] and
                      prototypical [GPe -TI]) in both healthy and PD states
                      [1].Firstly, we found that multiple parameter combinations
                      can fit the data. We functionally re-classified these PD and
                      healthy network models on the basis of two dynamical
                      features: suppression of GPi activity and susceptibility of
                      the BG network to oscillate in the presence of cortical
                      input. These features were chosen because task execution
                      requires GPi suppression while oscillations in the STN-GPe
                      subnetwork are characteristic of PD. We found that most
                      putative pathological networks showed insufficient
                      suppression of GPi activity and high susceptibility to
                      oscillations whereas most putative healthy networks showed
                      sufficient suppression of GPi activity and low
                      susceptibility to oscillations. This is consistent with
                      experimental data that shows that lack of GPi suppression
                      [2] or oscillations [3,4] is correlated with Parkinsonian
                      symptoms such as stymied movement and tremor. A small
                      fraction of networks, however, in both cases show deficiency
                      in only one of the features. This could indicate the
                      configurations of healthy networks that might be more
                      pathology prone and in contrast configurations of
                      pathological networks that might be easier to push into a
                      healthy state. Further analysis of estimated BG connectivity
                      revealed that transitions between the putative PD and
                      healthy networks were possible by modifying the strength of
                      the relevant projections. Most of the transitions involved
                      changes in corticostriatal, striatopallidal and
                      pallidopallidal projections. Finally, the variance observed
                      in the functional classification of putative pathological
                      and healthy networks might hint at the variance observed in
                      manifestation of Parkinson's disease
                      (PD).AcknowledgementsKlinische Forschergruppe (KFO219, TP12)
                      of the Deutsche Forschungsgemeinschaft; Helmholtz
                      Association, EuroSPIN and Erasmus Mundus Joint Doctorate
                      Programme.References1.Abdi A, Mallet N, Mohamed FY, Sharott
                      A, Dodson PD, Nakamura KC, Suri S, Avery SV, Larvin JT,
                      Garas FN, Garas SN, Vinciati F, Morin S, Bezard E, Baufreton
                      J, Magill PJ: Prototypic and Arkypallidal Neurons in the
                      Dopamine-Intact External Globus Pallidus . J Neurosci 2015,
                      37(17): 6667-6688.2. Boraud T, Bezard E, Bioulac B, Gross
                      CE: Ratio of inhibited-to-activated pallidal neurons
                      decreases dramatically during passive limb movement in the
                      MPTP-treated monkey. J. Physiol 2000, 83(3): 1760-1763. 3.
                      Chen CC, Litvak V, Gilbertson T, Kühn A, Lu CS, Lee ST,
                      Tsai CH, Tisch S, Limousin P, Hariz M, Brown P: Excessive
                      synchronization of basal ganglia neurons at 20 Hz slows
                      movement in Parkinson's disease. Exp Neurol. 2007, 205(1):
                      214-221.4. Moran A, Bergman H, Israel Z, Bar-Gad I:
                      Subthalamic nucleus functional organization revealed by
                      parkinsonian neuronal oscillations and synchrony. Brain
                      2008, 131(Pt-12): 3395-3409.},
      month         = {Mar},
      date          = {2017-03-24},
      organization  = {12th International Basal Ganglia
                       Society Meeting, Merida (Mexico), 24
                       Mar 2017 - 31 Mar 2017},
      subtyp        = {After Call},
      cin          = {INM-6 / IAS-6 / INM-10},
      cid          = {I:(DE-Juel1)INM-6-20090406 / I:(DE-Juel1)IAS-6-20130828 /
                      I:(DE-Juel1)INM-10-20170113},
      pnm          = {574 - Theory, modelling and simulation (POF3-574) / 571 -
                      Connectivity and Activity (POF3-571) / 331 - Signalling
                      Pathways and Mechanisms in the Nervous System (POF2-331)},
      pid          = {G:(DE-HGF)POF3-574 / G:(DE-HGF)POF3-571 /
                      G:(DE-HGF)POF2-331},
      typ          = {PUB:(DE-HGF)24},
      url          = {https://juser.fz-juelich.de/record/829370},
}