[MURG] Computational Model of Cognitive Deficits in Medicated and Non-medicated Parkinsonism. (fwd from frankmj@grey.colorado.edu)

[Eugen Leitl]

----- Forwarded message from "Michael J. Frank" <frankmj at grey.colorado.edu> -----

From: "Michael J. Frank" <frankmj at grey.colorado.edu>
Date: Tue, 16 Mar 2004 15:04:33 +0100
To: comp-neuro at neuroinf.org
Subject: Computational Model of Cognitive Deficits in Medicated and Non-medicated
 Parkinsonism.
Reply-To: "Michael J. Frank" <frankmj at grey.colorado.edu>

Apologies for multiple postings.

Readers of this list may be interested in the following preprint, to 
appear in the Journal of Cognitive Neuroscience:

http://psych.colorado.edu/~frankmj/papers/BG_DA_model.preprint.pdf

Frank, M.J. (in press). Dynamic dopamine modulation in the basal ganglia:
A neurocomputational account of cognitive deficits in medicated and
non-medicated Parkinsonism. Journal of Cognitive Neuroscience.


  Abstract:

  Dopamine (DA) depletion in the basal ganglia (BG) of Parkinson's
  patients gives rise to both frontal-like and implicit learning
  impairments. Dopaminergic medication alleviates some cognitive
  deficits but impairs those that depend on intact areas of the BG,
  apparently due to DA ``overdose''. These findings are difficult to
  accommodate with verbal theories of BG/DA function, owing to
  complexity of system dynamics: DA dynamically modulates function in
  the BG, which is itself a modulatory system. This paper presents a
  neural network model that instantiates key biological properties and
  provides insight into the underlying role of DA in the BG during
  learning and execution of cognitive tasks.  Specifically, the BG
  modulates the execution of ``actions'' (e.g., motor responses and
  working memory updating) that are being considered in different
  parts of frontal cortex.  Phasic changes in DA, which occur during
  error feedback, dynamically modulate the BG threshold for
  facilitating/suppressing a cortical command in response to
  particular stimuli.  Reduced dynamic range of DA explains Parkinson
  and DA overdose deficits with a single underlying dysfunction,
  despite overall differences in raw DA levels.  Simulated
  Parkinsonism and medication effects provide a theoretical basis for
  behavioral data in probabilistic classification and reversal tasks.
  The model also provides novel testable predictions for
  neuropsychological and pharmacological studies, and motivates
  further investigation of BG/DA interactions with prefrontal cortex
  in working memory.





----- End forwarded message -----
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