Acute effects of cocaine on the neurobiology of cognitive control

Garavan, Hugh; Kaufman, Jacqueline; Hester, Robert

doi:10.1098/rstb.2008.0106

Cited by 131 publications

(101 citation statements)

References 80 publications

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“…Cocaine appears to have a direct effect on the neurobiology underlying impulse control. After an intravenous injection of cocaine, cocaine users actually showed an improvement in a motor response inhibition task and concomitant increased activation in their right dorsolateral and inferior frontal cortices (Garavan et al, 2008). Because these areas are considered to be important in impulse control, this observation suggests that some of the acute effects of cocaine could in fact mediate a transient reversal of the chronic hypofunction in impulse control circuitry.…”

Section: Ventral Striatum/dorsal Striatum/thalamus: Voluntary To Habimentioning

confidence: 79%

Erratum: Neurocircuitry of Addiction

Koob¹,

Volkow²

2010

Neuropsychopharmacol

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Drug addiction is a chronically relapsing disorder that has been characterized by (1) compulsion to seek and take the drug, (2) loss of control in limiting intake, and (3) emergence of a negative emotional state (eg, dysphoria, anxiety, irritability) reflecting a motivational withdrawal syndrome when access to the drug is prevented. Drug addiction has been conceptualized as a disorder that involves elements of both impulsivity and compulsivity that yield a composite addiction cycle composed of three stages: 'binge/intoxication', 'withdrawal/negative affect', and 'preoccupation/anticipation' (craving). Animal and human imaging studies have revealed discrete circuits that mediate the three stages of the addiction cycle with key elements of the ventral tegmental area and ventral striatum as a focal point for the binge/intoxication stage, a key role for the extended amygdala in the withdrawal/negative affect stage, and a key role in the preoccupation/anticipation stage for a widely distributed network involving the orbitofrontal cortex-dorsal striatum, prefrontal cortex, basolateral amygdala, hippocampus, and insula involved in craving and the cingulate gyrus, dorsolateral prefrontal, and inferior frontal cortices in disrupted inhibitory control. The transition to addiction involves neuroplasticity in all of these structures that may begin with changes in the mesolimbic dopamine system and a cascade of neuroadaptations from the ventral striatum to dorsal striatum and orbitofrontal cortex and eventually dysregulation of the prefrontal cortex, cingulate gyrus, and extended amygdala. The delineation of the neurocircuitry of the evolving stages of the addiction syndrome forms a heuristic basis for the search for the molecular, genetic, and neuropharmacological neuroadaptations that are key to vulnerability for developing and maintaining addiction.

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Section: Ventral Striatum/dorsal Striatum/thalamus: Voluntary To Habimentioning

confidence: 79%

Erratum: Neurocircuitry of Addiction

Koob¹,

Volkow²

2010

Neuropsychopharmacol

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“…Based on this theory, IAD subjects are supposed to recover much harder from the distressing thoughts caused by their error responses. Third, the disruption of ACC functioning contributes to impaired cognitive control in IAD through impairment in its performance-monitoring function [52]. In the presence of response conflict, people are known to sometimes make impulsive errors based on partial, incomplete analysis of the stimulus.…”

Section: Discussionmentioning

confidence: 99%

Impaired Error-Monitoring Function in People with Internet Addiction Disorder: An Event-Related fMRI Study

Dong¹,

Shen²,

Huang³

et al. 2013

Eur Addict Res

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Background: Internet addiction disorder (IAD) is rapidly becoming a prevalent mental health concern around the world. The neurobiological underpinnings of IAD should be studied to unravel the potential heterogeneity. This study was set to investigate the error-monitoring ability in IAD subjects. Methods: Fifteen IAD subjects and 15 healthy controls (HC) participated in this study. Participants were asked to perform a fast Stroop task that may show error responses. Behavioral and neurobiological results in relation to error responses were compared between IAD subjects and HC. Results: Compared to HC, IAD subjects showed increased activation in the anterior cingulate cortex (ACC) and decreased activation in the orbitofrontal cortex following error responses. Significant correlation was found between ACC activation and the Internet addiction test scores. Conclusions: IAD subjects show an impaired error-monitoring ability compared to HC, which can be detected by the hyperactivation in ACC in error responses.

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“…In addition to the pleasurable effects, acute cocaine has also been shown to improve cognition in humans (Garavan et al 2008) and enhance learning and memory in laboratory rodents (Wood et al 2007). However, these procognitive effects during initial cocaine exposure may be responsible for the formation of maladaptive drug-context/-cue associations that may facilitate the development of compulsive drug-seeking behavior.…”

Section: Cocainementioning

confidence: 99%

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

2016

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It has long been hypothesized that conditioning mechanisms play major roles in addiction. Specifically, the associations between rewarding properties of drugs of abuse and the drug context can contribute to future use and facilitate the transition from initial drug use into drug dependency. On the other hand, the self-medication hypothesis of drug abuse suggests that negative consequences of drug withdrawal result in relapse to drug use as an attempt to alleviate the negative symptoms. In this review, we explored these hypotheses and the involvement of the hippocampus in the development and maintenance of addiction to widely abused drugs such as cocaine, amphetamine, nicotine, alcohol, opiates, and cannabis. Studies suggest that initial exposure to stimulants (i.e., cocaine, nicotine, and amphetamine) and alcohol may enhance hippocampal function and, therefore, the formation of augmented drug-context associations that contribute to the development of addiction. In line with the self-medication hypothesis, withdrawal from stimulants, ethanol, and cannabis results in hippocampus-dependent learning and memory deficits, which suggest that an attempt to alleviate these deficits may contribute to relapse to drug use and maintenance of addiction. Interestingly, opiate withdrawal leads to enhancement of hippocampus-dependent learning and memory. Given that a conditioned aversion to drug context develops during opiate withdrawal, the cognitive enhancement in this case may result in the formation of an augmented association between withdrawalinduced aversion and withdrawal context. Therefore, individuals with opiate addiction may return to opiate use to avoid aversive symptoms triggered by the withdrawal context. Overall, the systematic examination of the role of the hippocampus in drug addiction may help to formulate a better understanding of addiction and underlying neural substrates.Addiction is a major worldwide health problem that results in maladaptive behavioral changes, some that can last a lifetime. This behavioral plasticity, often times maladaptive, must be associated changes in neural plasticity. In fact, it has been noted multiple times that there is a high degree of overlap between the neurobiology of learning and memory and the neurobiology of addiction

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Acute effects of cocaine on the neurobiology of cognitive control

Cited by 131 publications

References 80 publications

Erratum: Neurocircuitry of Addiction

Erratum: Neurocircuitry of Addiction

Impaired Error-Monitoring Function in People with Internet Addiction Disorder: An Event-Related fMRI Study

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

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