The role of the striatopallidal and
extended amygdala systems in drug addiction
by
Koob GF
Department of Neuropharmacology,
CVN-7, Scripps Research Institute,
La Jolla, California 92037, USA.
gkoob@scripps.edu
Ann N Y Acad Sci 1999 Jun 29; 877:445-60

ABSTRACT

Evidence suggests that the acute reinforcing actions of drugs of abuse may be mediated by specific elements of the striatopallidal and extended amygdala systems. These include the shell of the nucleus accumbens, the central nucleus of the amygdala, and the sublenticular extended amygdala. Chronic administration of drugs of abuse, including cocaine, amphetamines, nicotine, alcohol, and tetrahydrocannabinol leads to an increasing dysregulation of brain reward systems that is characterized by decreases in reward function. Withdrawal from chronic administration of cocaine, amphetamine, nicotine, alcohol, and tetrahydrocannabinol raises thresholds for brain stimulation reward. Neurochemical elements in the extended amygdala may mediate these changes, including decreases in dopamine and serotonin neurotransmission in the nucleus accumbens and increases in the brain-stress neurotransmitter, corticotropin-releasing factor, in the central nucleus of the amygdala. The combination of decreases in function of neurotransmitters involved in the positive-reinforcing properties of drugs of abuse with recruitment of brain-stress systems within the extended amygdala provides a powerful mechanism for allostatic changes in hedonic set point that can lead to the compulsive drug-seeking and drug-taking behavior characteristic of addiction.

MAOIs
Opioids
Reward
Cocaine
Nicotine
Cannabis
Dopamine
Amygdala
Dopaminergics
Zero tolerance
NMDA antagonists
The guilt-free soldier
The hedonic treadmill
Addiction and reward
The nucleus accumbens
The neural basis of addiction
Inner workings of the amygdala

Refs
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