Connectionists: New paper: Neurocomputational model of tonic and phasic dopamine in cognitive deficits in Parkinson's

[Mark A. Gluck]

Dear Colleagues,

A PDF of our new neurocomputational modeling  paper:

Guthrie, M., Myers, C. E., & Gluck, M. A. (2009/In press). A 
neurocomputational model of tonic and phasic dopamine in action 
selection: A comparison with cognitive deficits in Parkinson's 
disease. Behavioral Brain Research.

has been posted online to our lab web site at:

	http://www.gluck.edu/pdf/BBR_5811.pdf

[if you have trouble with this URL, it is also linked from our home page
at  http://www.gluck.edu/ ]

An ABSTRACT for this paper is as follows:

	The striatal dopamine signal has multiple facets; tonic 
level, phasic rise and fall, and variation of the phasic rise/fall 
depending on the expectation of reward/punishment.We have developed a 
network model of the striatal direct pathway using an ionic current 
level model of the medium spiny neuron that incorporates currents 
sensitive to changes in the tonic level of dopamine. The model 
neurons in the network learn action selection based on a novel set of 
mathematical rules that incorporate the phasic change in the dopamine 
signal. This network model is capable of learning to perform a 
sequence learning task that in humans is thought to be dependent on 
the basal ganglia. When both tonic and phasic levels of dopamine are 
decreased, as would be expected in unmedicated Parkinson's disease 
(PD), the model reproduces the deficits seen in a human PD group off 
medication. When the tonic level is increased to normal, but with 
reduced phasic increases and decreases in response to reward and 
punishment, respectively, as would be expected in PD medicated with 
L-Dopa, the model again reproduces the human data. These findings 
support the view that the cognitive dysfunctions seen in Parkinson's 
disease are not solely either due to the decreased tonic level of 
dopamine or to the decreased responsiveness of the phasic dopamine 
signal to reward and punishment, but to a combination of the two 
factors that varies dependent on disease stage and medication status.


As always, we welcome and appreciate comments, feedback, and pointers 
to relevant published or unpublished research. This paper is one in a 
series of forthcoming theoretical papers that seek to better 
understand the nature of the cognitive deficits in Parkison's disease 
through modeling  frontal and/or striatal dopamine function in 
learning and decision making.

Regards, Mark Gluck
___________________________________
Dr. Mark A. Gluck,  Professor  
   Co-Director, Rutgers Memory Disorders Project  
Center for Molecular  and Behavioral Neuroscience
Rutgers University                                
197 University Ave.                                   
Newark, New Jersey  07102                  

   Web:  http://www.gluck.edu
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