Instrumental performance following a shift in primary motivation depends on incentive learning.

1992 ◽  
Vol 18 (3) ◽  
pp. 236-250 ◽  
Author(s):  
Bernard Balleine
1983 ◽  
Vol 35 (3b) ◽  
pp. 249-263 ◽  
Author(s):  
Anthony Dickinson ◽  
D. J. Nicholas

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.


1992 ◽  
Vol 20 (4) ◽  
pp. 322-328 ◽  
Author(s):  
Matias Lopez ◽  
Bernard Balleine ◽  
Anthony Dickinson

Author(s):  
Richard J. Beninger

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.


Author(s):  
Richard J. Beninger

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.


Author(s):  
Elena Torna ◽  
Elena Smith ◽  
Meagan Lamothe ◽  
Dr. Bobbi Langkamp-Henken ◽  
Dr. Jeanette M Andrade

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