Current perspectives on incentive salience and applications to clinical disorders

Olney, Jeffrey J.; Warlow, Shelley M.; Naffziger, Erin E.; Berridge, Kent

doi:10.1016/j.cobeha.2018.01.007

Cited by 122 publications

(60 citation statements)

References 112 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, cues can become unnaturally strong motivators of drug-seeking behavior in addiction (4,8,94,95) and NAc cholinergic interneurons have been linked to addiction-like behaviors (96,97). Depression can be characterized by avolitional symptoms (94,98), and NAc cholinergic interneurons have been linked to depressionlike behavior (35). These results, therefore, have implications for the understanding and treatment of these and other diseases marked by maladaptive motivation.…”

Section: Discussionmentioning

confidence: 99%

Nucleus accumbens cholinergic interneurons oppose cue-motivated behavior

Collins

Aitken

Huang

et al. 2019

Preprint

View full text Add to dashboard Cite

Background: Environmental reward-predictive stimuli provide a major source of motivation for adaptive reward pursuit behavior. This cue-motivated behavior is known to be mediated by the nucleus accumbens core (NAc). The cholinergic interneurons in the NAc are tonically active and densely arborized and, thus, well-suited to modulate NAc function. But their causal contribution to adaptive behavior remains unknown. Here we investigated the function of NAc cholinergic interneurons in cue-motivated behavior.Methods: To do this, we used chemogenetics, optogenetics, pharmacology, and a translationally analogous Pavlovian-to-instrumental transfer behavioral task designed to assess the motivating influence of a reward-predictive cue over reward-seeking actions in male and female rats. Results:The data show that NAc cholinergic interneuron activity is necessary and sufficient to oppose the motivating influence of appetitive cues. Chemogenetic inhibition of NAc cholinergic interneurons augmented cue-motivated behavior. Optical stimulation of acetylcholine release from NAc cholinergic interneurons prevented cues from invigorating reward-seeking behavior, an effect that was mediated by activation of β2-containing nicotinic acetylcholine receptors.Conclusions: Thus, NAc cholinergic interneurons provide a critical regulatory influence over adaptive cue-motivated behavior and, therefore, are a potential therapeutic target for the maladaptive cue-motivated behavior that marks many psychiatric conditions, including addiction and depression. Collins et al 3Environmental reward-predictive stimuli provide a major source of motivation for adaptive reward pursuit behaviors (1). This incentive motivational value can become dysfunctional in many psychiatric disease states (2). Indeed, it can become amplified allowing cues to become potent triggers for maladaptive compulsive overeating (3), alcohol abuse (4-7), or drug seeking (8-12).Stress, anxiety, and depression (13-16) can also disrupt the motivating influence of appetitive cues, resulting in dampened or inappropriate motivation. The nucleus accumbens core (NAc) has been implicated in cue-motivated behavior (17)(18)(19). But little is known about the function of the major NAc neuromodulator acetylcholine. Such information is crucial given the purported importance of cholinergic signaling in many mental illnesses (20,21).Cholinergic interneurons provide the primary, though not exclusive (22), source of acetylcholine in the NAc (23). Despite comprising only 1-2% of the population, these large-bodied, tonically active neurons are densely arborized (24-29), making them ideally suited to modulate NAc function and associated behaviors. Cholinergic interneurons have also been shown to locally regulate striatal dopamine release (30-32). NAc cholinergic signaling is elevated under conditions that discourage vigorous reward seeking, such as satiety (33, 34), and has been implicated in anxiety-and depression-like states (35, 36) marked by blunted motivation. Cholinergic interneurons are transien...

show abstract

Section: Discussionmentioning

confidence: 99%

Nucleus accumbens cholinergic interneurons oppose cue-motivated behavior

Collins

Aitken

Huang

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…In the MELD framework, instrumental outcome value is based on both the motivational salience of an outcome (the degree to which the outcome elicits an implicit approach or avoidance response) and an individual's cognitive desire or aversion towards the outcome (the degree to which the outcome is explicitly represented as desirable or undesirable; Berridge et al, 2009;Olney, Warlow, Naffziger, & Berridge, 2018). The lower the instrumental outcome value, the lower the likelihood that the instrumental action will be carried out (i.e., inaction may result).…”

Section: Environmental and Motivational Factors Determine Instrumentamentioning

confidence: 99%

Pavlovian and Instrumental Conditioning and Their Mutual Influence in Major Depressive Disorder: The Mood and Emotional Learning Dynamics (MELD) Framework

Terpstra¹,

Rm²

2020

Preprint

View full text Add to dashboard Cite

Major Depressive Disorder (MDD) poses a significant burden for individuals and society. It compromises quality of life, disrupts productivity, and strains social relationships. Pavlovian and instrumental conditioning play an important role in psychopathology, yet the independent and joint contributions of these forms of emotional learning to depressed mood are not well understood. In particular, studies of Pavlovian conditioning and Pavlovian-instrumental transfer (PIT) in MDD are few. Studying PIT in MDD may improve our understanding of how emotional learning influences depressive symptoms that is more reflective of how Pavlovian and instrumental conditioning operate in the real world. In this review, we first provide a narrative summary of past research investigating emotional learning in MDD, including computational modeling approaches. Based on these findings, we then build on an existing theoretical framework characterizing emotional learning and decision making in depression by incorporating the potential influence of Pavlovian conditioned cues on instrumental behaviour in individuals experiencing depressed mood. Specifically, we propose that, in MDD, adaptive instrumental behaviours are interrupted by the exaggerated inhibitory influence of aversive Pavlovian cues and insufficiently invigorated by appetitive Pavlovian cues. We conclude with recommendations for future research investigating emotional learning in MDD.

show abstract

“…Models of schizophrenia have also been shown to display reduced positive bias for a greater reward value [81], whilst other studies show they do not show anhedonia-like deficits [82]. In addition, pharmacological agents have been identified as specific to influencing either 'wanting' or 'liking' separately, or in opposite directions [83]. This indicates mechanisms underlying hedonic experience, motivation and learning can be separated, implying that -while they may interact -rewardprocessing deficits are not monolithic, and each needs to be investigated individually.…”

Section: Relationship Between Affective Biases and Other Reward-relatmentioning

confidence: 99%

“…A third major component of reward processing deficits in depressed patients involves motivation for reward. For many years motivational processes and hedonic experience have been confounded when assessing clinical populations, potentially contributing to the difficulty in assessing consummatory anhedonia, as typical self-report measures would not adequately separate 'wanting' from deficits in 'liking' [83]. Motivational processes integrate the biological need for a reward, and learning and memory of a reward-associated stimulus to drive goal-directed actions to gain the reward [173].…”

Section: Motivationmentioning

confidence: 99%

Affective biases and their interaction with other reward-related deficits in rodent models of psychiatric disorders

Lewis

Benn

Dwyer

et al. 2019

Behavioural Brain Research

View full text Add to dashboard Cite

Major depressive disorder (MDD) is one of the leading global causes of disability. Symptoms of MDD can vary person to person, and current treatments often fail to alleviate the poor quality of life that patients experience. One of the two, core diagnostic criteria for MDD is the loss of interest in previously pleasurable activities, which suggests a link between the disease aetiology and reward processing. Cognitive impairments are also common in patients with MDD, and more recently, emotional processing deficits known as affective biases have been recognised as a key feature of the disorder. Studies in animals have found similar affective biases related to reward. In this review we consider these affective biases in the context of other reward-related deficits and examine how affective biases associated with learning and memory may interact with the wider behavioural symptoms seen in MDD. We discuss recent developments in how analogues of affective biases and other aspects of reward processing can be assessed in rodents, as well as how these behaviours are influenced in models of MDD. We subsequently discuss evidence for the neurobiological mechanisms contributing to one or more reward-related deficits in preclinical models of MDD, identified using these behavioural assays. We consider how the relationships between these selective behavioural assays and the neurobiological mechanisms for affective bias and reward processing could be used to identify potential treatment strategies.

show abstract

Current perspectives on incentive salience and applications to clinical disorders

Cited by 122 publications

References 112 publications

Nucleus accumbens cholinergic interneurons oppose cue-motivated behavior

Nucleus accumbens cholinergic interneurons oppose cue-motivated behavior

Pavlovian and Instrumental Conditioning and Their Mutual Influence in Major Depressive Disorder: The Mood and Emotional Learning Dynamics (MELD) Framework

Affective biases and their interaction with other reward-related deficits in rodent models of psychiatric disorders

Contact Info

Product

Resources

About