Addiction and brain reward and antireward pathways

Area of Science:

• Neuroscience
• Psychiatry
• Pharmacology

Background:

• Addictive drugs are voluntarily self-administered and enhance brain reward circuitry, causing a 'high'.
• The core reward circuit involves the ventral tegmental area, nucleus accumbens, and ventral pallidum, functioning beyond simple hedonic tone to include attention, expectancy, and motivation.
• Hedonic dysregulation in these circuits is a potential cause of addiction.

Purpose of the Study:

• To explore the common mechanisms of addictive drugs on brain reward circuitry.
• To elucidate the neurobiological underpinnings of addiction progression and relapse.
• To review current knowledge for developing pharmacotherapeutic treatments.

Main Methods:

• Review of neurobiological mechanisms of addictive drugs.
• Analysis of animal self-administration studies and human neuroimaging data.
• Examination of neurochemical and neuroanatomical pathways involved in reward, dependence, craving, and relapse.

Main Results:

• All addictive drugs enhance dopaminergic function in the nucleus accumbens, regulating self-administration.
• Addiction progresses from reward-driven to habit-driven behavior, correlating with anatomical shifts from ventral to dorsal striatal control.
• Distinct brain circuits and neurotransmitters mediate pleasure, physical dependence, craving, and relapse triggers (drugs, stress, cues).

Conclusions:

• Addiction involves a hypodopaminergic dysfunctional state in the reward circuitry, supported by neuroimaging.
• Serotonergic, opioid, endocannabinoid, GABAergic, and glutamatergic systems also play roles in addiction.
• Knowledge of neurobiology informs the development of pharmacotherapeutic strategies for addiction treatment.