1 / 20

Bischoff(Grethe)-Arbib Basal Ganglia Modeling

Bischoff(Grethe)-Arbib Basal Ganglia Modeling. Presented by James Bonaiuto. Amanda Bischoff (Grethe)’s Thesis. Models the basal ganglia (and some cortical areas) in three tasks: Elbow flexion-extension Reciprocal aiming Sequential arm movements

Download Presentation

Bischoff(Grethe)-Arbib Basal Ganglia Modeling

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Bischoff(Grethe)-Arbib Basal Ganglia Modeling Presented by James Bonaiuto

  2. Amanda Bischoff (Grethe)’s Thesis • Models the basal ganglia (and some cortical areas) in three tasks: • Elbow flexion-extension • Reciprocal aiming • Sequential arm movements • Dopamine levels were modified to model the effects of Parkinson’s

  3. Hypothesis on Basal Ganglia Function • Basal Ganglia • Indirect pathway – movement inhibition • Direct pathway – provides next sensory state to cortex • Cortex • Preparatory areas – project to indirect path • Movement-related areas – project to direct pathway

  4. Model Overview - Cortex • Pre-SMA • Projects sequential information to SMA and indirect pathway • SMA • Contains information on the overall sequence • Keeps track of which movement is next • Project current movement to MC and direct pathway of basal ganglia • Project next movement to premovement population in MC and indirect pathway of basal ganglia • Motor Cortex • Carries out motor command • Handles fine-tuning of movement • Projects motor parameters to brainstem and direct pathway of basal ganglia

  5. Next Sensory State Information • Why aren’t the basal ganglia responsible for movement initiation? • Crutcher & Alexander (1990) – movement related putamen neurons fire an average of 33 ms after the onset of a movement (after activation of MC – 56ms later, and SMA – 80 ms later) • Mink & Thach (1991b) – movement-related activity in GPe and GPi is also late • Turner & Anderson (1997) – GP neurons rarely change discharge before activity of agonist muscles

  6. Basic Model • Segregated direct (movement)/indirect (preparation) pathways • Neat modeling trick: • To model up/down states of putamen neurons, the time constant is a sigmoid of the membrane potential • Same trick is used later to slowdown the cortex in the absence of dopamine

  7. Elbow Flexion-Extension

  8. Elbow Flexion-Extension - Results <Demonstration>

  9. Reciprocal Aiming • Winstein et al. (1997) – Stylus tapping between two targets of varying sizes • Fitt’s Law – speed/accuracy tradeoff • ID=log2(2A/W) • MT=a+bID • Parkinson’s patients • Slower overall time • Constrained trajectory • Reached to smaller area of target • Predictions: • Slower speed is due to inability of BG to release inhibition of movement • Decrease in SMA and MC activity causes reduction in speed and variation of movement

  10. Reciprocal Aiming - Model • Input: target positions in joint space • Problem when targets overlap in joint space • SMA_INH prepares upcoming movement – BG inhibits before appropriate • WTA– only fires in relation to movement in preparation • SMA_MVT receives info from both targets • Inhibition from SMA_INH – only responds to current target • MC_MVT • Encodes joint coordinates - converted to Cartesian space • Movement time calculated from firing rate

  11. Reciprocal Aiming - Results • Normal - Qualitatively similar to Winstein et al.’s (1997) control data • 50% Dopamine • No contact with target, no pause between movements • Because neural part of model taking less time than arm • Hypothesis: slowdown in putamen function may cause slowdown in cortex too • Changed time constants of SMA and MC to depend on dopamine level • With dopamine depletion – takes longer for neurons to reach maximum and maximum is less than with dopamine (because of longer time constant) • Reduction in MC firing rates causes delays between movements • Caused restricted arm trajectory – lower velocity

  12. Reciprocal Aiming Results SMA-Proper Motor Cortex

  13. Reciprocal Aiming Results Putamen GPe STN GPi SNc

  14. Reciprocal Aiming Results 50% Dopamine 20% Dopamine Normal

  15. Sequential Arm Movements • Extends SMA module for a sequence of three movements • Tanji & Shima (1994) – SMA neurons selective for sequence order, others selective for movement no matter where it was in a sequence • Tanji & Mushiake (1996) - Pre-SMA active for visual stimuli – indicate sequence to be performed

  16. Sequential Arm Movements - Model • Pre-SMA • Now selective for different sequence permutations • SMA • New population selective for different sequence permutations and subsequences • After the current movement begins, SMA_INH primes SMA_MVT for the next movement • MC_MVT needs to reach a threshold firing rate to produce target for movement generator • Hardcoded relationships between SMA_SEQ, SMA_MVT and SMA_INH

  17. Sequential Arm Movements - Results SMA-Proper Motor Cortex • Seq123 and seq12 active until target 1 reached • Seq12 primes target 2 neurons in SMA_PROPER_INH and seq23 • Target 1 reached – seq23 reaches full activation • Seq23 primes target 3 neurons in SMA_PROPER_INH • Drop dopamine - seq123 is active longer • MC_MVT peaks for each movement lower than for previous one - each movement depends on activation from previous movement

  18. Sequential Arm Movements - Results Putamen GPe STN GPi SNc

  19. Sequential Arm Movements - Results • Reduce dopamine • Beginnings of pause between each submovement • Akinesia - took longer to initiate 1st movement • Bradykinesia – each movement take longer and longer • Indirect pathway is overactive (inhibits motor programs), direct pathway is less capable of responding to current motor command • Slower time constant and higher GPi inhibition -> SMA doesn’t know status of current motor program so doesn’t command the next movement Normal 50% Dopamine 20% Dopamine

  20. Discussion • Can the same model do all three tasks? • Reciprocal aiming and flexion-extension can be cast as 2 movement sequences • Requires new weights for the SMA_SEQ12 and SMA_SEQ21 populations • How can these weights be learned? • The future work section lists the inclusion of cortico-STN projections • The GPR model includes these, but has an opposite take on the basal ganglia function (action selection) • Are these views reconcilable?

More Related