Effects of quinolinic acid-induced lesions of the orbital prefrontal cortex on inter-temporal choice: a quantitative analysis

Kheramin, S.; Body, S.; Mobini, Sirous; Ho, M.-Y.; Velázquez-Martínez, David N.; Bradshaw, C. M.; Szabadi, E.; Deakin, Bill; Anderson, Ian M.

doi:10.1007/s00213-002-1228-6

Cited by 102 publications

(56 citation statements)

References 38 publications

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“…This suggests that manipulating the AcbC only affects behavior that synthesizes both delay and magnitude. Such a conclusion appears to conflict with previous results, which suggest that the AcbC is involved in sensitivity to delay per se (Kheramin et al, 2002; Bezzina et al, 2007; da Costa Araújo et al, 2010). However, the studies by Kheramin et al (2002) and Bezzina et al (2007) used tasks that manipulated both delay and magnitude, and had no explicit measure of delay sensitivity in isolation.…”

Section: Discussioncontrasting

confidence: 79%

“…Such a conclusion appears to conflict with previous results, which suggest that the AcbC is involved in sensitivity to delay per se (Kheramin et al, 2002; Bezzina et al, 2007; da Costa Araújo et al, 2010). However, the studies by Kheramin et al (2002) and Bezzina et al (2007) used tasks that manipulated both delay and magnitude, and had no explicit measure of delay sensitivity in isolation. On the other hand, the study by da Costa Araújo et al (2010) used a task that independently assessed sensitivity to delay, but did not directly manipulate the AcbC.…”

Section: Discussioncontrasting

confidence: 79%

“…Conversely, the role of the OFC is less clear. Some studies have found that lesions increase delay discounting (Mobini et al, 2002; Kheramin et al, 2002; Kheramin et al, 2003; Rudebeck et al, 2006), one has found that lesions decrease discounting (Winstanley et al, 2004), and some have found no effect (Mariano et al, 2009; Finger et al, 2011; Abela et al, 2013; Jo et al, 2013). These discrepant findings have been suggested to be the result of procedural differences (Zeeb et al, 2010) and/or the regional specificity of the lesions (Mar et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…Both delay and magnitude sensitivity are important components of delay discounting (Ho et al, 1999; Killeen, 2009; Logue et al, 1984), and determining the neurological underpinnings of these components may increase our understanding of discounting and its role in various behavioral disorders. Mathematical analysis of delay discounting data has suggested that the AcbC may modulate sensitivity to delay, while the OFC may modulate sensitivity to delay and magnitude (Kheramin et al, 2002; Bezzina et al, 2007; but see Galtress & Kirkpatrick, 2010). However, because these studies used a delay discounting task that manipulated delay and magnitude simultaneously, they were unable to directly measure sensitivity to delay or magnitude in isolation.…”

Section: Introductionmentioning

confidence: 99%

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

Moschak

Mitchell

2014

Behavioural Brain Research

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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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Section: Discussioncontrasting

confidence: 79%

Section: Discussioncontrasting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Moschak

Mitchell

2014

Behavioural Brain Research

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“…Because sensitivity to delayed reinforcement and sensitivity to reinforcer magnitude independently influence discounting of a reinforcer (Ho, Mobini, Chiang, Bradshaw, & Szabadi, 1999), we applied quantitative analyses (e.g., exponential discounting function) to determine if DA receptors and Glu receptors within NAcc differentially alter these parameters. Quantitative analyses have been used previously to determine the effects of excitotoxic lesions (Bezzina et al, 2007, 2008, 2009; da Costa Araújo et al, 2009; Kheramin et al, 2002; Valencia-Torres et al, 2012) and pharmacological manipulations (Yates et al, 2015, 2017a, 2017b) on delay discounting. By applying quantitative analyses in the current study, we sought to determine the precise mechanisms by which NAcc DA or Glu receptors mediate discounting.…”

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confidence: 99%

Effects of intra-accumbal administration of dopamine and ionotropic glutamate receptor drugs on delay discounting performance in rats.

Yates

Bardo

2017

Behavioral Neuroscience

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Nucleus accumbens core (NAcc) has been implicated in impulsive choice, as measured in delay discounting. The role of dopamine (DA) in impulsive choice has received considerable attention, whereas glutamate (Glu) has recently been shown to be an important mediator of discounting. However, research has not examined how DA or Glu receptors in NAcc mediate different aspects of delay discounting performance, i.e., (1) sensitivity to reinforcer magnitude and (2) sensitivity to delayed reinforcement. Adult male Sprague Dawley rats were first trained in a delay discounting task, in which the delay to a large magnitude food reinforcer increased across blocks of trials. Following behavioral training, rats received bilateral implantation of guide cannulae into NAcc. Half of the rats (n = 12) received infusions of the DA-selective ligands SKF 38393 (D1-like agonist: 0.03 or 0.1 μg), SCH 23390 (D1-like antagonist: 0.3 or 1.0 μg), quinpirole (D2-like agonist: 0.3 or 1.0 μg), and eticlopride (D2-like antagonist: 0.3 or 1.0 μg). The other half received infusions of the ionotropic Glu ligands MK-801 (NMDA uncompetitive antagonist: 0.3 or 1.0 μg), AP-5 (NMDA competitive antagonist: 0.3 or 1.0 μg), ifenprodil (noncompetitive antagonist at NR2B-containing NMDA receptors: 0.3 or 1.0 μg), and CNQX (AMPA competitive antagonist: 0.2 or 0.5 μg). Results showed that SCH 23390 (0.3 μg) decreased sensitivity to reinforcer magnitude without altering impulsive choice, whereas ifenprodil (1.0 μg) decreased sensitivity to delayed reinforcement (i.e., impulsive choice). The current results show that DA and NMDA receptors in NAcc mediate distinct aspects of discounting performance.

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Delay Discounting and Impulsive Choice in the Rat

Mar

Robbins

2007

CP Neuroscience

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Delay discounting refers to the degree to which immediate outcomes exhibit more influence over behavior than outcomes which are delayed. Impulsive choice, in the context of delay discounting, is generally considered as an increased preference for immediate over delayed outcomes, even where the delayed outcomes are more advantageous. In the past decade, there has been increasing use of delay-discounting paradigms to elucidate the physiological, pharmacological, and behavioral aspects of the putative neural circuitry underlying impulsive choice. This unit describes the assessment of impulsive choice in the rat using a delay-discounting procedure involving an operant response choice between a small reinforcer delivered immediately and a larger reinforcer delivered after a delay, which is progressively increased within a session. Variations of some of the main task parameters are also discussed, as well as their significance and interpretation.

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Effects of quinolinic acid-induced lesions of the orbital prefrontal cortex on inter-temporal choice: a quantitative analysis

Cited by 102 publications

References 38 publications

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

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

Effects of intra-accumbal administration of dopamine and ionotropic glutamate receptor drugs on delay discounting performance in rats.

Delay Discounting and Impulsive Choice in the Rat

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