Editing Operant conditioning (section)

==Neurobiological correlates==
{{Further|Reward system}}
The first scientific studies identifying [[neuron]]s that responded in ways that suggested they encode for conditioned stimuli came from work by Mahlon deLong<ref>[http://jn.physiology.org/cgi/content/citation/34/3/414 "Activity of pallidal neurons during movement"], M.R. DeLong, ''J. Neurophysiol.'', 34:414–27, 1971</ref><ref name="RTR&MRD">Richardson RT, DeLong MR (1991): Electrophysiological studies of the function of the nucleus basalis in primates. In Napier TC, Kalivas P, Hamin I (eds), ''The Basal Forebrain: Anatomy to Function'' (''Advances in Experimental Medicine and Biology''), vol. 295. New York, Plenum, pp. 232–252</ref> and by R.T. Richardson.<ref name=RTR&MRD/> They showed that [[nucleus basalis]] neurons, which release [[acetylcholine]] broadly throughout the [[cerebral cortex]], are activated shortly after a conditioned stimulus, or after a primary reward if no conditioned stimulus exists. These neurons are equally active for positive and negative reinforcers, and have been shown to be related to [[neuroplasticity]] in many [[cerebral cortex|cortical]] regions.<ref>PNAS 93:11219-24 1996, Science 279:1714–8 1998</ref> Evidence also exists that [[Dopamine#Functions in the brain|dopamine]] is activated at similar times.<ref>{{Cite journal |last=Rozenfeld |first=Eyal |last2=Parnas |first2=Moshe |date=2024-12-06 |title=Neuronal circuit mechanisms of competitive interaction between action-based and coincidence learning |url=https://www.science.org/doi/10.1126/sciadv.adq3016 |journal=Science Advances |volume=10 |issue=49 |pages=eadq3016 |doi=10.1126/sciadv.adq3016 |pmc=11623277 |pmid=39642217}}</ref> There is considerable evidence that dopamine participates in both reinforcement and aversive learning.<ref>Neuron 63:244–253, 2009, Frontiers in Behavioral Neuroscience, 3: Article 13, 2009</ref> Dopamine pathways project much more densely onto [[frontal cortex]] regions. [[Cholinergic]] projections, in contrast, are dense even in the posterior cortical regions like the [[primary visual cortex]]. A study of patients with [[Parkinson's disease]], a condition attributed to the insufficient action of dopamine, further illustrates the role of dopamine in positive reinforcement.<ref>Michael J. Frank, Lauren C. Seeberger, and Randall C. O'Reilly (2004) "By Carrot or by Stick: Cognitive Reinforcement Learning in Parkinsonism," ''Science'' 4, November 2004</ref> It showed that while off their medication, patients learned more readily with aversive consequences than with positive reinforcement. Patients who were on their medication showed the opposite to be the case, positive reinforcement proving to be the more effective form of learning when dopamine activity is high.

A neurochemical process involving dopamine has been suggested to underlie reinforcement.  When an organism experiences a reinforcing stimulus, [[dopamine]] pathways in the brain are activated. This network of pathways "releases a short pulse of dopamine onto many [[dendrites]], thus broadcasting a global reinforcement signal to [[postsynaptic neuron]]s."<ref>{{cite journal|last1=Schultz|first1=Wolfram|year=1998|title=Predictive Reward Signal of Dopamine Neurons|journal=The Journal of Neurophysiology|volume=80|issue=1|pages=1–27|doi=10.1152/jn.1998.80.1.1|pmid=9658025|s2cid=52857162 |doi-access=free}}</ref> This allows recently activated synapses to increase their sensitivity to efferent (conducting outward) signals, thus increasing the probability of occurrence for the recent responses that preceded the reinforcement. These responses are, statistically, the most likely to have been the behavior responsible for successfully achieving reinforcement. But when the application of reinforcement is either less immediate or less contingent (less consistent), the ability of dopamine to act upon the appropriate synapses is reduced.