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Dopamine Contributions to Motivational Vigor and Reinforcement Driven Learning.

Record Type:	Language materials, manuscript : Monograph/item
Title/Author:	Dopamine Contributions to Motivational Vigor and Reinforcement Driven Learning./
Author:	Hamid, Arif.
Description:	1 online resource (206 pages)
Notes:	Source: Dissertation Abstracts International, Volume: 78-07(E), Section: B.
Subject:	Neurosciences. -
Online resource:	click for full text (PQDT)
ISBN:	9781369588149

Dopamine Contributions to Motivational Vigor and Reinforcement Driven Learning.
Hamid, Arif.

Dopamine Contributions to Motivational Vigor and Reinforcement Driven Learning. - 1 online resource (206 pages)

Source: Dissertation Abstracts International, Volume: 78-07(E), Section: B.

Thesis (Ph.D.)--University of Michigan, 2016.

Includes bibliographical references

Brain mechanisms for reinforcement learning and adaptive decision-making are widely accepted to critically involve the basal ganglia (BG) and the neurotransmitter dopamine (DA). DA is a key modulator of synaptic plasticity within the striatum, critically regulating neurophysiological adaptations for normal reinforcement driven learning, and maladaptive changes during disease conditions (e.g. drug addiction, Parkinson's disease). Activity in midbrain DA cells are reported to encode errors in reward prediction, providing a learning signal to guide future behaviors. Yet, dopamine is also a key modulatory of motivation, invigorating current behavior. Prevailing theories of DA emphasize its role in either affecting current performance, or modulating reward-related learning.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2018

Mode of access: World Wide Web

ISBN: 9781369588149Subjects--Topical Terms:

593561
Neurosciences.
Index Terms--Genre/Form:

554714
Electronic books.

Dopamine Contributions to Motivational Vigor and Reinforcement Driven Learning.
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100 1 $a Hamid, Arif. $3 1186616
245 1 0 $a Dopamine Contributions to Motivational Vigor and Reinforcement Driven Learning.
264 0 $c 2016
300 $a 1 online resource (206 pages)
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500 $a Source: Dissertation Abstracts International, Volume: 78-07(E), Section: B.
500 $a Adviser: Joshua Damien Berke.
502 $a Thesis (Ph.D.)--University of Michigan, 2016.
504 $a Includes bibliographical references
520 $a Brain mechanisms for reinforcement learning and adaptive decision-making are widely accepted to critically involve the basal ganglia (BG) and the neurotransmitter dopamine (DA). DA is a key modulator of synaptic plasticity within the striatum, critically regulating neurophysiological adaptations for normal reinforcement driven learning, and maladaptive changes during disease conditions (e.g. drug addiction, Parkinson's disease). Activity in midbrain DA cells are reported to encode errors in reward prediction, providing a learning signal to guide future behaviors. Yet, dopamine is also a key modulatory of motivation, invigorating current behavior. Prevailing theories of DA emphasize its role in either affecting current performance, or modulating reward-related learning.
520 $a This thesis will present data aimed at resolving gaps in the literature for how DA makes simultaneous contributions to dissociable learning and motivational processes. Specifically, I argue that striatal DA fluctuations signal a single decision variable: a Value function (an ongoing estimate of discounted future rewards) that is used for motivational decision making ('Is It worth it?') and that abrupt deflections in this value function serve as temporal-difference reward prediction errors used for reinforcement/learning ("repeat action?"). These DA prediction errors may be causally involved in strengthening some, but not all, valuation mechanisms. Furthermore, DA activity on the midbrain-forebrain axis indicate a dissociation between DA cell bodies and their striatal terminals. I propose that this is an adaptive computational strategy, whereby DA targets tailor release to their own computational requirements, potentially converting an RPE-like spike signal into a motivational (value) message.
533 $a Electronic reproduction. $b Ann Arbor, Mich. : $c ProQuest, $d 2018
538 $a Mode of access: World Wide Web
650 4 $a Neurosciences. $3 593561
655 7 $a Electronic books. $2 local $3 554714
690 $a 0317
710 2 $a ProQuest Information and Learning Co. $3 1178819
710 2 $a University of Michigan. $b Neuroscience. $3 1186617
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10391602 $z click for full text (PQDT)