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1.
Behav Brain Sci ; 44: e30, 2020 08 26.
Article in English | MEDLINE | ID: mdl-32843105

ABSTRACT

Most authors who discuss willpower assume that everyone knows what it is, but our assumptions differ to such an extent that we talk past each other. We agree that willpower is the psychological function that resists temptations - variously known as impulses, addictions, or bad habits; that it operates simultaneously with temptations, without prior commitment; and that use of it is limited by its cost, commonly called effort, as well as by the person's skill at executive functioning. However, accounts are usually not clear about how motivation functions during the application of willpower, or how motivation is related to effort. Some accounts depict willpower as the perceiving or formation of motivational contingencies that outweigh the temptation, and some depict it as a continuous use of mechanisms that interfere with re-weighing the temptation. Some others now suggest that impulse control can bypass motivation altogether, although they refer to this route as habit rather than willpower.It is argued here that willpower should be recognized as either or both of two distinct functions, which can be called resolve and suppression. Resolve is based on interpretation of a current choice as a test case for a broader set of future choices, which puts at stake more than the outcome of the current choice. Suppression is inhibiting valuation of (modulating) and/or keeping attention from (filtering) immediate alternatives to a current intention. Perception of current choices as test cases for broader outcomes may result in reliable preference for these outcomes, which is experienced as an effortless habit - a successful result of resolve, not an alternative method of self-control. Some possible brain imaging correlates are reviewed.


Subject(s)
Motivation , Self-Control , Behavior, Addictive/prevention & control , Behavior, Addictive/psychology , Brain/physiology , Executive Function , Female , Humans , Impulsive Behavior , Male
2.
Neuropharmacology ; 99: 658-64, 2015 Dec.
Article in English | MEDLINE | ID: mdl-26334786

ABSTRACT

Exposure to drugs of abuse can produce many neurobiological changes which may lead to increased valuation of rewards and decreased sensitivity to their costs. Many of these behavioral alterations are associated with activity of D2-expressing medium spiny neurons in the striatum. Additionally, Bdnf in the striatum has been shown to play a role in flexible reward-seeking behavior. Given that voluntary aerobic exercise can affect the expression of these proteins in healthy subjects, and that exercise has shown promise as an anti-addictive therapy, we set out to quantify changes in D2 and Bdnf expression in methamphetamine-exposed rats given access to running wheels. Sixty-four rats were treated for two weeks with an escalating dose of methamphetamine or saline, then either sacrificed, housed in standard cages, or given free access to a running wheel for 6 weeks prior to sacrifice. Rats treated with methamphetamine ran significantly greater distances than saline-treated rats, suggesting an augmentation in the reinforcement value of voluntary wheel running. Transcription of Drd2 and Bdnf was assessed via RT-qPCR. Protein expression levels of D2 and phosphorylation of the TrkB receptor were measured via western blot. Drd2 and Bdnf mRNA levels were impacted independently by exercise and methamphetamine, but exposure to methamphetamine prior to the initiation of exercise blocked the exercise-induced changes seen in rats treated with saline. Expression levels of both proteins were elevated immediately after methamphetamine, but returned to baseline after six weeks, regardless of exercise status.


Subject(s)
Central Nervous System Stimulants/pharmacology , Corpus Striatum/drug effects , Frontal Lobe/drug effects , Methamphetamine/pharmacology , Running/physiology , Animals , Blotting, Western , Brain-Derived Neurotrophic Factor/metabolism , Corpus Striatum/metabolism , Frontal Lobe/metabolism , Gene Expression/drug effects , Gene Expression/physiology , Male , Motor Activity/drug effects , Motor Activity/physiology , Phosphorylation/drug effects , RNA, Messenger/metabolism , Rats, Long-Evans , Receptor, trkB/metabolism , Receptors, Dopamine D2/metabolism , Sedentary Behavior , Volition
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