The Addicted Brain (original) (raw)
Related papers
Imaging the addicted brain.pdf
http://jnm.snmjournals.org/content/45/11/13N.citation This article and updated information are available at: http://jnm.snmjournals.org/site/subscriptions/online.xhtml Information about subscriptions to JNM can be found at: http://jnm.snmjournals.org/site/misc/permission.xhtml
of the reward and motivation circuits while decreasing the activity in the cognitive control circuit. This contributes to an inability to inhibit the drive to seek and consume the drug and results in compulsive drug intake. This model has implications for therapy, for it suggests a multi-prong approach that targets strategies to decrease the rewarding properties of drugs, to enhance the rewarding properties of alternative reinforcers, to interfere with conditioned-learned associations, and to strengthen cognitive control in the treatment of drug addiction.
The 'Metaphmaracology' of the Addicted Brain
Journal of the History of the Present, 2011
JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.
Bioscience, 1999
The dopamine pathway is helping researchers find their way through the addiction maze ur flourishing knowledge of the brain is in large part the product of research on addiction. Identifying what happens in the brain when a drug is inhaled, injected, or eaten, why it leads to compulsive drug seeking, and learning how to disrupt that process has seemed like the last best hope for a permanent fix for addiction. Which is why, according to Alan Leshner, director of the National Institute on Drug Abuse (NIDA), researchers know more about drugs in the brain than they know about anything else in the brain. Among the revelations: addiction is now seen to be a brain disease triggered by frequent use of drugs that change the biochemistry and anatomy of neurons and alter the way they work. Scientists have developed a basic model of addiction that presents these changes as the desperate attempt of the brain to carry on business-as-usual-to make neurons less responsive to the drugs and so restore homeostasis-while under extreme chemical siege. But the adaptations the drugs force on the brain can be long term or even permanent. With sustained drug use, the brain adapts to this saturation bombardment, and giving up drugs leaves it bereft and demanding a return to the new homeostasis. Thus, even the brains of people who have quit using drugs and urgently wish to stay clean remain vulnerable to relapse. Deprived addicts are no longer seeking to get high, they just want to feel normal. Genetic factors, environmental factors, and-most important-the intricate and still mysterious interaction of the two are assumed to be fundamental to the addiction process. But a great many critical details are emerging from studies of events in the brain.
Toward a critical neuroscience of 'addiction'
BioSocieties, 2010
Early to mid-twentieth century studies on the neurophysiology of the role of conditioned cues in relapse, conducted at the Addiction Research Center in Lexington, Kentucky, were the historical antecedents to today's neuroimaging studies. Attempts in the 1940s to see 'what's going on in the brains of these addicts' were formative for the field, as was foundational work done in the 1940s and 1950s by Abraham Wikler on conditioned cues, the role of what he called the 'limbic system' in relapse, and possible uses of narcotic antagonists to prevent relapse by extinguishing cues. This article sketches the historical context in order to situate continuities between historical antecedents and a current ethnographic case study focused on current neuroimaging studies of the role of 'craving' -and neural processes that precede conscious 'craving' and occur 'outside awareness' -in relapse conducted by Anna Rose Childress at the Treatment Research Center in Philadelphia, Pennsylvania. The article showcases the incommensurability between claims that 'addiction' is a matter of individual choice, and claims that it is a neurochemical disorder disruptive of volition. Neuroscientists offer scientific vocabulary and imagery that both shape and respond to the social experience of addiction. The conclusion considers the value of moving toward a critical neuroscience more cognizant of the social worlds in which 'addiction' occurs, not in the restricted sense of 'social factors' but through awareness of the social-situational contexts and relationships within which 'addictions' are experienced and studied.
Neurocircuitry of addiction.pdf
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.