It’s all in your head: The neurocircuitry of addiction

According to the National Institute on Drug Abuse, abuse of tobacco, alcohol, and illicit drugs costs over $600 billion annually due to crime, lost work productivity, and healthcare expenses.  Brain chemistry can be one of the reasons why it is so difficult to conquer addictions.

Did you know that addictive drugs and normal learned behaviors stimulate the same neural pathways?  As such, the neurological reward and emotional sense of pleasure associated with the achievement of normal biological cues are also stimulated by addictive drugs.  The difference between the two is that drugs cause a much higher degree of neuronal pathway stimulation and neurotransmitter release.  This flood of neurotransmitters causes prolonged changes in the brains’ neurocircuitry responsible for sensing satisfaction and reward; and appears to play a key role in addiction.

There has been extensive research illustrating the neurotransmitters and neural adaptations involved in addiction.  Simply put, the development of addiction occurs when neuronal projections from the ventral tegmental area (VTA) increase dopamine signaling within the pleasure sensing nucleus accumbens.  This pathway is reinforced through repeated exposures to the substance, which causes the prefrontal cortex to learn and eventually repeat the behavior that led to the neurotransmitter release.

The neural circuits of the VTA, nucleus accumbens, and prefrontal cortex are critical in learning both natural and addictive behavior.

Here is a closer look at the neurocircuitry of addiction and how dopamine and glutamate are key neurotransmitters involved (Figure 1):

  1. Upon exposure to a naturally rewarding stimulus or a drug, there is an increase in
    Figure 1. Dopamine and glutamate are key players in the neurocircuitry of addiction.

    Figure 1. Dopamine and glutamate are key players in the neurocircuitry of addiction.

    dopamine signaling from the VTA to the nucleus accumbens.  The nucleus accumbens ‘perceives’ this dopamine signal and measures the ‘goodness’ of the reward based upon the size of the dopamine release.

  2. Glutamate projections from the nucleus accumbens instruct the prefrontal cortex to remember the environment and behaviors which lead to the occurrence of ‘goodness’.
  3. Excess signaling of glutamate neurons in the prefrontal cortex stimulates the nucleus accumbens, triggering addiction-seeking behaviors at the expense of naturally rewarding behaviors.

Addiction occurs as the result of dopamine signaling in the nucleus accumbens, and glutamate projections from the prefrontal cortex are key plays in drug seeking and relapse.  Glutamate and dopamine both play roles in addiction, and assessing imbalances can help successfully treat addictive behaviors.

Guest author: Jennifer Farley is a manager of the Clinical Support & Education Department at NeuroScience, Inc. and one of the resident experts in psychiatric disorders.

References:
Baker DA, Xi ZX, Shen H, Swanson CJ, Kalivas PW. (2002). The origin and neuronal function of in vivo nonsynaptic glutamate. J Neurosci, 22(20):9134-41.
Goldstein RZ, Volkow ND. (2002). Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex. Am J Psychiatry, 159(10):1642-52.
Kalivas PW, Volkow ND.  (2005). The neural basis of addiction: a pathology of motivation and choice. Am J Psychiatry, 162(8):1403-13.
Roberts AJ, Koob GF. (1997). The neurobiology of addiction: an overview. Alcohol Health Res World,  21(2):101-6.
http://www.drugabuse.gov/related-topics/trends-statistics
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