On the resilience of reward cues attentional salience to reward devaluation, time, incentive learning, and contingency remapping.

2021 ◽  
Author(s):  
Matteo De Tommaso ◽  
Massimo Turatto
Keyword(s):  
Incentive Learning

Schizophrenia, Parkinson’s disease, and attention deficit hyperactivity disorder

2018 ◽  
Author(s):  
Richard J. Beninger
Keyword(s):  
Parkinson’S Disease ◽  
Attention Deficit Hyperactivity Disorder ◽  
Parkinson's Disease ◽  
Attention Deficit ◽  
Antipsychotic Treatment ◽  
Incentive Learning ◽  
Dopaminergic Drugs ◽  
Dopaminergic Neurotransmission ◽  
Hyperactivity Disorder ◽  
Incentive Value

Schizophrenia, Parkinson’s disease, and attention deficit hyperactivity disorder (ADHD) discusses how hyperactive dopaminergic neurotransmission appears to underlie schizophrenia’s positive symptoms, loss of dopaminergic neurons in adulthood leads to Parkinson’s disease, and dopamine neuron hypofunction in childhood and adolescence may underlie ADHD. Positive schizophrenia symptoms may arise from excessive incentive learning that is gradually lost with antipsychotic treatment. Declarative learning and memory may contribute to delusions based on excessive incentive learning. Loss of responsiveness to environmental stimuli in Parkinson’s may result from a decrease of their conditioned incentive value and inverse incentive learning. Conditioned incentive stimuli not encountered while in a state of decreased dopaminergic neurotransmission may retain their incentive value, producing apparent kinesia paradoxa. Dopamine hypofunction in juveniles does not lead to hypokinesia but may result in loss of incentive learning that focuses attention. Pro-dopaminergic drugs have a calming effect in ADHD, presumably because they reinstate normal incentive learning.

Dopamine and inverse incentive learning

2018 ◽  
Author(s):  
Richard J. Beninger
Keyword(s):  
Dopamine Neurons ◽  
Incentive Learning ◽  
Repeated Presentation ◽  
Aversive Stimuli ◽  
Incentive Value ◽  
Conditioned Incentive Stimuli

Dopamine and inverse incentive learning explains that dopamine determines an incentive–value continuum. Novel and intense stimuli innately produce rapid dopamine neurons activation followed by inhibition. The repeated presentation of novel stimuli leads to a loss of this effect. Aversive stimuli, biologically important by definition, often deactivate dopamine neurons and may produce inverse incentive learning, leading to conditioned inverse incentive stimuli with decreased ability to elicit approach and other responses. The offset of aversion may increase the firing of dopamine neurons producing incentive learning about safety-related stimuli. Habituation to stimuli enhances their ability to produce inverse incentive learning, suggesting that inverse incentive learning may occur during habituation. In the end, there may be no “neutral” stimuli, only stimuli that lie on a continuum of incentive value from strong conditioned incentive stimuli to strong conditioned inverse incentive stimuli with most of the things we encounter in day-to-day life falling in between.

EFFECTS OF CANNABINOID RECEPTOR LIGANDS ON INCENTIVE LEARNING IN RATS

1998 ◽  
Vol 9 (Supplement) ◽  
pp. S23 ◽  
Author(s):  
F. C. Chaperon ◽  
R. Aubree ◽  
M. H. Thiebot
Keyword(s):  
Cannabinoid Receptor ◽  
Incentive Learning ◽  
Receptor Ligands

Differential Impairments in Incentive Learning Caused by First‐ and Second‐ Generation Antipsychotic Drugs

2016 ◽  
Author(s):  
Matthew Florczynski
Keyword(s):  
Neural Control ◽  
First Generation ◽  
Antipsychotic Drugs ◽  
Second Generation ◽  
Operant Chamber ◽  
Incentive Learning ◽  
Dopamine Receptor Antagonists ◽  
Natural Response ◽  
Second Generation Antipsychotic ◽  
First And Second Generation

Schizophrenia is a neuropsychiatric disorder characterized by increased function of dopamine in the brain.  Dopamine release is a natural response to reward.  It promotes incentive learning (IL), a process by which neutral stimuli acquire the ability to elicit approach and other responses.  A recent model characterizes dopamine‐mediated IL as a progressive process with early and late stages accompanied by a shift in neural control from the nucleus accumbens (NAc) to the dorsolateral striatum (DLS).  A parallel can be drawn to differences in regionally specific neural responses generated by first‐ and second‐generation antipsychotic drugs (APDs) used to treat schizophrenia.  APDs are dopamine receptor antagonists, but first‐generation APDs affect the NAc and DLS while second‐generation APDs affect primarily the NAc.  We compared the effects of APDs on IL. Rats (N = 48) were trained to press a lever forfood pellets in an operant chamber.  Intraperitoneal injections (1 hr before testing) of the first‐generation APD haloperidol (0,0.05,0.10,0.20 mg/kg) or of the second‐generation APD risperidone (0,0.20,0.40,0.80 mg/kg) induced dose‐dependent suppression of lever pressing on days 1‐4, with the highest dose groups failing to demonstrate any evidence of previous learning on day 5 when tested drug‐free.  On days 16‐20 haloperidol induced a day‐to‐day suppression not seen with risperidone.  The results suggest that the effects of first‐ and second‐generation APDs on learning processes putatively mediated by the NAc and DLS can be differentiated experimentally.  The findings imply that APDs may differentially affect IL inpatients with schizophrenia.  

4.  Differential Impairments in Incentive Learning Caused by First‐ and Second‐ Generation Antipsychotic Drugs

2016 ◽  
Author(s):  
Matthew Florczynski
Keyword(s):  
Neural Control ◽  
First Generation ◽  
Antipsychotic Drugs ◽  
Second Generation ◽  
Operant Chamber ◽  
Incentive Learning ◽  
Dopamine Receptor Antagonists ◽  
Natural Response ◽  
Second Generation Antipsychotic ◽  
First And Second Generation

Schizophrenia is a neuropsychiatric disorder characterized by increased function of dopamine in the brain.  Dopamine release is a natural response to reward.  It promotes incentive learning (IL), a process by which neutral stimuli acquire the ability to elicit approach and other responses.  A recent model characterizes dopamine‐mediated IL as a progressive process with early and late stages accompanied by a shift in neural control from the nucleus accumbens (NAc) to the dorsolateral striatum (DLS).  A parallel can be drawn to differences in regionally specific neural responses generated by first‐ and second‐generation antipsychotic drugs (APDs) used to treat schizophrenia.  APDs are dopamine receptor antagonists, but first‐generation APDs affect the NAc and DLS while second‐generation APDs affect primarily the NAc.  We compared the effects of APDs on IL. Rats (N = 48) were trained to press a lever for food pellets in an operant chamber.  Intraperitoneal injections (1 hr before testing) of the first‐generation APD haloperidol (0,0.05,0.10,0.20 mg/kg) or of the second‐generation APD risperidone (0,0.20,0.40,0.80 mg/kg) induced dose‐dependent suppression of lever pressing on days 1‐4, with the highest dose groups failing to demonstrate any evidence of previous learning on day 5 when tested drug‐free.  On days 16‐20, haloperidol induced a day‐to‐day suppression not seen with risperidone.  The results suggest that the effects of first‐ and second‐generation APDs on learning processes putatively mediated by the NAc and DLS can be differentiated experimentally.  The findings imply that APDs may differentially affect IL inpatients with schizophrenia.

Irrelevant Incentive Learning during Instrumental Conditioning: The Role of the Drive-Reinforcer and Response-Reinforcer Relationships

1983 ◽  
Vol 35 (3b) ◽  
pp. 249-263 ◽  
Author(s):  
Anthony Dickinson ◽  
D. J. Nicholas
Keyword(s):  
Lever Press ◽  
Instrumental Conditioning ◽  
Convincing Evidence ◽  
Incentive Learning ◽  
Instrumental Performance ◽  
Test Drive ◽  
Sodium Appetite ◽  
Drive State ◽  
Sodium Solution

Four experiments investigated the processes by which a motivationally-induced change in the value of the training reinforcer affects instrumental performance. Initially, thirsty rats were trained to lever press for either a sodium or non-sodium solution. In Experiment I sodium-trained rats responded faster in extinction following the induction of a sodium appetite, but not following either food or water deprivation. Thus, enhanced extinction performance depends upon the relevance of the training reinforcer to the test drive state. The remaining experiments examined the role of the instrumental contingency. Animals received response-contingent presentations of one solution alternated either within (Experiments II and III) or between sessions (Experiment IV) with non-contingent presentations of another solution. Neither procedure yielded convincing evidence that contingent sodium presentations generated more responding in extinction under a sodium appetite than did non-contingent sodium presentations. On the basis of these results, we argue that the instrumental contingency itself does not play a major role in this irrelevant incentive effect.

scholarly journals Differential dependence of Pavlovian incentive motivation and instrumental incentive learning processes on dopamine signaling

2011 ◽  
Vol 18 (7) ◽  
pp. 475-483 ◽  
Author(s):  
K. M. Wassum ◽  
S. B. Ostlund ◽  
B. W. Balleine ◽  
N. T. Maidment
Keyword(s):  
Incentive Motivation ◽  
Learning Processes ◽  
Incentive Learning ◽  
Dopamine Signaling

Differential involvement of the endocannabinoid system in short- and long-term expression of incentive learning supported by nicotine in rats

2006 ◽  
Vol 189 (1) ◽  
pp. 59-69 ◽  
Author(s):  
Benoît Forget ◽  
Sandrine Barthélémy ◽  
Françoise Saurini ◽  
Michel Hamon ◽  
Marie-Hélène Thiébot
Keyword(s):  
Endocannabinoid System ◽  
Incentive Learning ◽  
Short And Long Term ◽  
Differential Involvement
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