41. ^  _**a** _ _**b** _ Berridge KC (April 2012).  "From prediction error to incentive salience: mesolimbic computation of reward motivation"  . _Eur. J. Neurosci_ . **35** (7): 1124–1143.  doi  "Doi \(identifier\)") :  10.1111/j.1460-9568.2012.07990.x  .  PMC  "PMC \(identifier\)")  3325516  .  PMID  "PMID \(identifier\)")  22487042  . " Here I discuss how mesocorticolimbic mechanisms generate the motivation component of incentive salience. Incentive salience takes Pavlovian learning and memory as one input and as an equally important input takes neurobiological state factors (e.g. drug states, appetite states, satiety states) that can vary independently of learning. Neurobiological state changes can produce unlearned fluctuations or even reversals in the ability of a previously learned reward cue to trigger motivation. Such fluctuations in cue-triggered motivation can dramatically depart from all previously learned values about the associated reward outcome. ... Associative learning and prediction are important contributors to motivation for rewards. Learning gives incentive value to arbitrary cues such as a Pavlovian conditioned stimulus (CS) that is associated with a reward (unconditioned stimulus or UCS). Learned cues for reward are often potent triggers of desires. For example, learned cues can trigger normal appetites in everyone, and can sometimes trigger compulsive urges and relapse in addicts.
Cue-triggered 'wanting' for the UCS
A brief CS encounter (or brief UCS encounter) often primes a pulse of elevated
motivation to obtain and consume more reward UCS. This is a signature feature
of incentive salience.
Cue as attractive motivational magnets
When a Pavlovian CS+ is attributed with incentive salience it not only
triggers 'wanting' for its UCS, but often the cue itself becomes highly
attractive – even to an irrational degree. This cue attraction is another
signature feature of incentive salience ... Two recognizable features of
incentive salience are often visible that can be used in neuroscience
experiments: (i) UCS-directed 'wanting' – CS-triggered pulses of intensified
'wanting' for the UCS reward; and (ii) CS-directed 'wanting' – motivated
attraction to the Pavlovian cue, which makes the arbitrary CS stimulus into a
motivational magnet. "

42. ** ^  ** Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (eds.). _Molecular Neuropharmacology: A Foundation for Clinical Neuroscience_ (2nd ed.). New York: McGraw-Hill Medical. pp. 147–148, 367, 376.  ISBN  "ISBN \(identifier\)")  978-0-07-148127-4   . " VTA DA neurons play a critical role in motivation, reward-related behavior (Chapter 15), attention, and multiple forms of memory. This organization of the DA system, wide projection from a limited number of cell bodies, permits coordinated responses to potent new rewards. Thus, acting in diverse terminal fields, dopamine confers motivational salience ("wanting") on the reward itself or associated cues (nucleus accumbens shell region), updates the value placed on different goals in light of this new experience (orbital prefrontal cortex), helps consolidate multiple forms of memory (amygdala and hippocampus), and encodes new motor programs that will facilitate obtaining this reward in the future (nucleus accumbens core region and dorsal striatum). In this example, dopamine modulates the processing of sensorimotor information in diverse neural circuits to maximize the ability of the organism to obtain future rewards. ...
The brain reward circuitry that is targeted by addictive drugs normally
mediates the pleasure and strengthening of behaviors associated with natural
reinforcers, such as food, water, and sexual contact. Dopamine neurons in the
VTA are activated by food and water, and dopamine release in the NAc is
stimulated by the presence of natural reinforcers, such as food, water, or a
sexual partner. ...
The NAc and VTA are central components of the circuitry underlying reward and
memory of reward. As previously mentioned, the activity of dopaminergic
neurons in the VTA appears to be linked to reward prediction. The NAc is
involved in learning associated with reinforcement and the modulation of
motoric responses to stimuli that satisfy internal homeostatic needs. The
shell of the NAc appears to be particularly important to initial drug actions
within reward circuitry; addictive drugs appear to have a greater effect on
dopamine release in the shell than in the core of the NAc. "

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59. ^  _**a** _ _**b** _ Ruffle JK (November 2014). "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". _Am. J. Drug Alcohol Abuse_ . **40** (6): 428–437.  doi  "Doi \(identifier\)") :  10.3109/00952990.2014.933840  .  PMID  "PMID \(identifier\)")  25083822  .  S2CID  "S2CID \(identifier\)")  19157711  . "
The strong correlation between chronic drug exposure and ΔFosB provides novel
opportunities for targeted therapies in addiction (118), and suggests methods
to analyze their efficacy (119). Over the past two decades, research has
progressed from identifying ΔFosB induction to investigating its subsequent
action (38). It is likely that ΔFosB research will now progress into a new era
– the use of ΔFosB as a biomarker. ...
Conclusions
ΔFosB is an essential transcription factor implicated in the molecular and
behavioral pathways of addiction following repeated drug exposure. The
formation of ΔFosB in multiple brain regions, and the molecular pathway