Partial inactivation of nucleus accumbens core decreases delay discounting in rats without affecting sensitivity to delay or magnitude

Travis M. Moschak, Suzanne Mitchell

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Increased preference for smaller, sooner rewards (delay discounting) is associated with several behavioral disorders, including ADHD and substance use disorders. However, delay discounting is a complex cognitive process and the relationship is unclear between the pathophysiology of the disorders and the component processes underlying delay discounting, including sensitivity to reinforcer delay and sensitivity to reinforcer magnitude. To investigate these processes, male Long Evans rats were trained in one of three tasks measuring sensitivity to delay, sensitivity to magnitude, or both (typical delay discounting task). After learning the task, animals were implanted with bilateral cannulae into either the nucleus accumbens core (AcbC) or the lateral orbitofrontal cortex (lOFC), both of which have been implicated in delay discounting. Upon recovering from the surgery, a baclofen/muscimol cocktail was infused to temporarily inactivate each of these two regions and task performance was assessed. Unlike previous studies showing that lesions of the AcbC increased delay discounting, partial inactivation of the AcbC decreased delay discounting, although it had no effects on the tasks independently assessing either sensitivity to delay or magnitude. The effects of AcbC inactivation were larger in animals that had low levels of delay discounting at baseline. Inactivation of the lOFC had no effects on behavior in any task. These findings suggest that the AcbC may act to promote impulsive choice in individuals with low impulsivity. Furthermore, the data suggest that the AcbC is able to modulate delay and magnitude sensitivity together, but not either of the two in isolation.

Original languageEnglish (US)
Pages (from-to)159-168
Number of pages10
JournalBehavioural Brain Research
Volume268
DOIs
StatePublished - Jul 15 2014

Fingerprint

Nucleus Accumbens
Prefrontal Cortex
Long Evans Rats
Muscimol
Baclofen
Delay Discounting
Impulsive Behavior
Task Performance and Analysis
Reward
Substance-Related Disorders
Learning

Keywords

  • Delay discounting
  • Impulsive choice
  • Intertemporal choice
  • Nucleus accumbens
  • Orbitofrontal cortex
  • Rat

ASJC Scopus subject areas

  • Behavioral Neuroscience
  • Medicine(all)

Cite this

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title = "Partial inactivation of nucleus accumbens core decreases delay discounting in rats without affecting sensitivity to delay or magnitude",
abstract = "Increased preference for smaller, sooner rewards (delay discounting) is associated with several behavioral disorders, including ADHD and substance use disorders. However, delay discounting is a complex cognitive process and the relationship is unclear between the pathophysiology of the disorders and the component processes underlying delay discounting, including sensitivity to reinforcer delay and sensitivity to reinforcer magnitude. To investigate these processes, male Long Evans rats were trained in one of three tasks measuring sensitivity to delay, sensitivity to magnitude, or both (typical delay discounting task). After learning the task, animals were implanted with bilateral cannulae into either the nucleus accumbens core (AcbC) or the lateral orbitofrontal cortex (lOFC), both of which have been implicated in delay discounting. Upon recovering from the surgery, a baclofen/muscimol cocktail was infused to temporarily inactivate each of these two regions and task performance was assessed. Unlike previous studies showing that lesions of the AcbC increased delay discounting, partial inactivation of the AcbC decreased delay discounting, although it had no effects on the tasks independently assessing either sensitivity to delay or magnitude. The effects of AcbC inactivation were larger in animals that had low levels of delay discounting at baseline. Inactivation of the lOFC had no effects on behavior in any task. These findings suggest that the AcbC may act to promote impulsive choice in individuals with low impulsivity. Furthermore, the data suggest that the AcbC is able to modulate delay and magnitude sensitivity together, but not either of the two in isolation.",
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AU - Moschak, Travis M.

AU - Mitchell, Suzanne

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N2 - Increased preference for smaller, sooner rewards (delay discounting) is associated with several behavioral disorders, including ADHD and substance use disorders. However, delay discounting is a complex cognitive process and the relationship is unclear between the pathophysiology of the disorders and the component processes underlying delay discounting, including sensitivity to reinforcer delay and sensitivity to reinforcer magnitude. To investigate these processes, male Long Evans rats were trained in one of three tasks measuring sensitivity to delay, sensitivity to magnitude, or both (typical delay discounting task). After learning the task, animals were implanted with bilateral cannulae into either the nucleus accumbens core (AcbC) or the lateral orbitofrontal cortex (lOFC), both of which have been implicated in delay discounting. Upon recovering from the surgery, a baclofen/muscimol cocktail was infused to temporarily inactivate each of these two regions and task performance was assessed. Unlike previous studies showing that lesions of the AcbC increased delay discounting, partial inactivation of the AcbC decreased delay discounting, although it had no effects on the tasks independently assessing either sensitivity to delay or magnitude. The effects of AcbC inactivation were larger in animals that had low levels of delay discounting at baseline. Inactivation of the lOFC had no effects on behavior in any task. These findings suggest that the AcbC may act to promote impulsive choice in individuals with low impulsivity. Furthermore, the data suggest that the AcbC is able to modulate delay and magnitude sensitivity together, but not either of the two in isolation.

AB - Increased preference for smaller, sooner rewards (delay discounting) is associated with several behavioral disorders, including ADHD and substance use disorders. However, delay discounting is a complex cognitive process and the relationship is unclear between the pathophysiology of the disorders and the component processes underlying delay discounting, including sensitivity to reinforcer delay and sensitivity to reinforcer magnitude. To investigate these processes, male Long Evans rats were trained in one of three tasks measuring sensitivity to delay, sensitivity to magnitude, or both (typical delay discounting task). After learning the task, animals were implanted with bilateral cannulae into either the nucleus accumbens core (AcbC) or the lateral orbitofrontal cortex (lOFC), both of which have been implicated in delay discounting. Upon recovering from the surgery, a baclofen/muscimol cocktail was infused to temporarily inactivate each of these two regions and task performance was assessed. Unlike previous studies showing that lesions of the AcbC increased delay discounting, partial inactivation of the AcbC decreased delay discounting, although it had no effects on the tasks independently assessing either sensitivity to delay or magnitude. The effects of AcbC inactivation were larger in animals that had low levels of delay discounting at baseline. Inactivation of the lOFC had no effects on behavior in any task. These findings suggest that the AcbC may act to promote impulsive choice in individuals with low impulsivity. Furthermore, the data suggest that the AcbC is able to modulate delay and magnitude sensitivity together, but not either of the two in isolation.

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