Rewards are both "liked" and "wanted," and those 2 words seem almost interchangeable. However, the brain circuitry that mediates the psychological process of "wanting" a particular reward is dissociable from circuitry that mediates the degree to which it is "liked." Incentive salience or "wanting," a form of motivation, is generated by large and robust neural systems that include mesolimbic dopamine. By comparison, "liking," or the actual pleasurable impact of reward consumption, is mediated by smaller and fragile neural systems, and is not dependent on dopamine. The incentive-sensitization theory posits the essence of drug addiction to be excessive amplification specifically of psychological "wanting," especially triggered by cues, without necessarily an amplification of "liking." This is because of long-lasting changes in dopamine-related motivation systems of susceptible individuals, called "neural sensitization." A quarter-century after its proposal, evidence has continued to grow in support the incentive-sensitization theory. Further, its scope is now expanding to include diverse behavioral addictions and other psychopathologies. (PsycINFO Database Record

Liking, wanting, and the incentive-sensitization theory of addiction.

Sleep abnormalities are associated with acute and chronic use of addictive substances. Although sleep complaints associated with use and abstinence from addictive substances are widely recognized, familiarity with the underlying sleep abnormalities is often lacking, despite evidence that these sleep abnormalities may be recalcitrant and impede good outcomes. Substantial research has now characterized the abnormalities associated with acute and chronic use of alcohol, cannabis, cocaine, and opiates. This review summarizes this research and discusses the clinical implications of sleep abnormalities in the treatment of substance use disorders.

/pdf/sleep-abnormalities-associated-with-alcohol-cannabis-cocaine-1a2dme54c7.pdf

Sleep abnormalities associated with alcohol, cannabis, cocaine, and opiate use: a comprehensive review

Experience with drugs of abuse (such as cocaine) produces powerful, long-lasting memories that may be important in the development and persistence of drug addiction. The neural mechanisms that mediate how and where these cocaine memories are encoded, consolidated and stored are unknown. Here we used conditioned place preference in mice to examine the precise neural circuits that support the memory of a cocaine-cue association (the "cocaine memory trace" or "cocaine engram"). We found that a small population of neurons (∼10%) in the lateral nucleus of amygdala (LA) were recruited at the time of cocaine-conditioning to become part of this cocaine engram. Neurons with increased levels of the transcription factor CREB were preferentially recruited or allocated to the cocaine engram. Ablating or silencing neurons overexpressing CREB (but not a similar number of random LA neurons) before testing disrupted the expression of a previously acquired cocaine memory, suggesting that neurons overexpressing CREB become a critical hub in what is likely a larger cocaine memory engram. Consistent with theories that coordinated postencoding reactivation of neurons within an engram or cell assembly is crucial for memory consolidation (Marr, 1971; Buzsaki, 1989; Wilson and McNaughton, 1994; McClelland et al., 1995; Girardeau et al., 2009; Dupret et al., 2010; Carr et al., 2011), we also found that post-training suppression, or nondiscriminate activation, of CREB overexpressing neurons impaired consolidation of the cocaine memory. These findings reveal mechanisms underlying how and where drug memories are encoded and stored in the brain and may also inform the development of treatments for drug addiction.

https://www.jneurosci.org/content/jneuro/34/42/14115.full.pdf

Manipulating a “Cocaine Engram” in Mice

Affective neuroscience research has revealed that reward contains separable components of ‘liking’, ‘wanting’, and learning. Here we focus on current ‘liking’ and ‘wanting’ findings and applications to clinical disorders. ‘Liking’ is the hedonic impact derived from a pleasant experience, and is amplified by opioid and related signals in discrete sites located in limbic-related brain areas. ‘Wanting’ refers to incentive salience, a motivation process for reward, and is mediated by larger systems involving mesocorticolimbic dopamine. Deficits in incentive salience may contribute to avolitional features of depression and related disorders, whereas deficits in hedonic impact may produce true anhedonia. Excesses in incentive salience, on the other hand, can lead to addiction, especially when narrowly focused on a particular target. Finally, a fearful form of motivational salience may even contribute to some paranoia symptoms of schizophrenia and related disorders.

Current perspectives on incentive salience and applications to clinical disorders.

The importance of considering polysubstance use: lessons from cocaine research.

Sleep disturbances and pain among individuals with prescription opioid dependence.

Aims

Functional magnetic resonance imaging research has attempted to elucidate the neurobehavioral underpinnings of cocaine dependence by evaluating differences in brain activation to cocaine and response inhibition cues between cocaine-dependent individuals and controls. This study investigated associations between task-related brain activation and cocaine use characteristics.



Design

Cross-sectional.



Setting

The Center for Biomedical Imaging at the Medical University of South Carolina, USA.



Participants

Fifty-one cocaine users (41 dependent).



Measurements

Brain activation to cocaine-cue exposure and Go No-Go tasks in six a priori selected brain regions of interest and cocaine use characteristics (i.e. cocaine dependence status, years of cocaine use, cocaine use in the past 90 days) assessed via standardized interviews.



Findings

Participants demonstrated elevated activation to cocaine (bilateral ventral striatum, dorsal caudate, amygdala) and response inhibition (bilateral anterior cingulate, insula, inferior frontal gyrus) cues in all hypothesized brain regions. Years of cocaine use was associated with task-related brain activation, with more years of cocaine use associated with greater activation to cocaine cues in right (F = 7.97, P = 0.01) and left (F = 5.47, P = 0.02) ventral striatum and greater activation to response inhibition cues in left insula (F = 5.10, P = 0.03) and inferior frontal gyrus (F = 4.12, P = 0.05) controlling for age, cocaine dependence status and cocaine use in the past 90 days.



Conclusions

Years of cocaine use may be more centrally related to cocaine cue and response inhibition brain activation than cocaine dependence diagnosis or amount of recent use.

The relationship between years of cocaine use and brain activation to cocaine and response inhibition cues

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Sleep disturbances and pain among individuals with prescription opioid dependence.

The relationship between years of cocaine use and brain activation to cocaine and response inhibition cues