Addiction and the brain antireward system Chapter uri icon. Overview; Identity; Additional Document Info; View All. scroll to property group menus. Drug addiction is conceptualized as chronic, relapsing compulsive use of drugs with significant dysregulation of brain hedonic systems. Koob GF, Le Moal M (). Addiction and the brain antireward system. Ann Rev Psychol 29– Koob GF, Stinus L, Le Moal M, Bloom FE (a).

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Neurobiological substrates for the dark side of compulsivity in addiction.

The neural substrates antirewward neuropharmacological mechanisms for btain negative motivational effects of drug withdrawal may involve disruption of the same neurochemical systems and neurocircuits implicated in the positive reinforcing effects of drugs of abuse, termed a within-system neuroadaptation. In a series of elegant studies by McGaugh, Roosendal, and colleagues, the basolateral amygdala was shown to mediate the memory-modulating effects of adrenal stress hormones, with a key role for noradrenergic activation.

Single cocaine exposure in vivo induces long-term potentiation in dopamine neurons. Although the emergence of a negative emotional state is not an established criterion of Substance Dependence defined by the Diagnostic and Statistical Manual of Mental Disorder4 th edition DSM-IV, [ 4 ]it is a reflection of what has been termed motivational withdrawal.

The neuropharmacological basis of reward. However, the view that drug addiction represents a simple break with homeostasis is not sufficient to explain a number of key elements of addiction.

Memory consolidation and the amygdala: J Exp Anal Behav. Annals of the New York Academy of Sciences 1, During ethanol withdrawal, extrahypothalamic CRF systems become hyperactive, with an increase in extracellular CRF within the central nucleus of the amygdala and bed nucleus of the stria terminalis of dependent rats [ 19586599 ], and this dysregulation of brain CRF systems is hypothesized to underlie both the enhanced anxiety-like behaviors and enhanced ethanol self-administration associated with ethanol withdrawal.


Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear. Drug Discov Today Ther Strat. Sterling P, Eyer J. University of Nebraska Press; Conversely, the basolateral amygdala is hypothesized to mediate consolidation of memories of emotionally arousing experiences via the nucleus accumbens, caudate addction, hippocampus, and entorhinal cortex [ 56 ].

Drug addiction has been conceptualized as a disorder that progresses from impulsivity to compulsivity in a collapsed cycle of addiction comprised of three stages: Studies on the neurocircuitry of fear conditioning show that auditory stimuli from the auditory cortex and pain from the somatosensory cortex converge on the lateral amygdala, which then projects to the central nucleus of the amygdala to elicit the various autonomic and behavioral responses to conditioned fear [ 50 ].

Behavioral and brain sciences 10 2, Post-training intra-basolateral amygdala infusions of norepinephrine enhance consolidation of memory for contextual fear conditioning. Much evidence from both human and animal studies supports antirward hypothesis that drugs of abuse can convey conditioned positive reinforcing properties and conditioned negative reinforcing properties.

Allostasis and allostatic load: At the same time, within the motivational circuits of the ventral striatum-extended amygdala, reward function decreases. Dopamine activity in the nucleus accumbens during consummatory phases of oral ethanol self-administration. Conditioned reinforcement as a measure of the rewarding properties of drugs.

Addiction and the brain antireward system.

Studies on duration of a late recovery period after chronic abuse of ethanol: Numerous studies have demonstrated the involvement of the extended amygdala CRF system in mediating the behavioral responses associated with fear and anxiety [ 40 ]. Addictikn conditioned reinforcing effects of stimuli associated with morphine reinforcement.

Markou A, Koob GF. A history of dependence in rats and mice can produce a prolonged elevation in ethanol self-administration in daily 30 min sessions long after acute withdrawal and detoxification [ 7072 ]. Different theoretical perspectives, ranging from experimental and social psychology to neurobiology, can be superimposed on these three stages, which are conceptualized as feeding into each other, becoming more intense, and andd from positive to negative reinforcement.


Central neural mechanisms that interrelate sensory and affective dimensions of pain. Roy A, Pandey SC.

Drugs and drug dependence. Animal models of drug craving and relapse continue to be developed and refined, but to date have largely reflected secondary sources of reinforcement such as conditioned reinforcement [ 5287 ]. Allostatic mechanisms also have been hypothesized to be involved in maintaining a functioning brain emotional system that has relevance for the pathology of addiction [ 42 ].

Effect of positive and negative affective stimuli and beverage cues on measures of craving in non treatment-seeking alcoholics.

Opioid peptide receptors in the ventral striatum, ventral tegmental area, and amygdala have been hypothesized to mediate the acute reinforcing effects of opioid and ethanol self-administration, largely based on the effects of opioid antagonists. The following articles are merged in Scholar.

The effects of 6-hydroxydopamine lesions of the nucleus accumbens and the mesolimbic dopamine system on oral self-administration of ethanol in the rat.

George Koob – Google Scholar Citations

Subsequent presentation of only the tone and odor elicited both the subjective effects of discomfort as well as the objective physical signs of withdrawal. Dopamine D3 receptor antagonism inhibits cocaine-seeking and cocaine-enhanced brain reward in rats. Much evidence indicates that drugs, thf more specifically psychostimulant drugs, can enhance cognitive performance.