More on neuroplasticity

Neuroplasticity: how our brains re-wire.

Researchers have now shown that long-term changes affect the brain even after drug use has ceased. This concept is especially important in light of the revolutionary idea of neuroplasticity, a conception that has overtaken the field of neuroscience in recent years. The overarching concept of neuroplasticity is that our brains are constantly changing and evolving. Whereas scientists in the field once believed that we were born with all of the brain cells that we would have in our entire life, we now understand that neurons are able to regenerate, and even more importantly, that our brain circuits are able to rewire as a result of experience.  Evidence from research of the past two decades offers support for this theory. Thompson showed that patients suffering from aphasia as a result of brain injury were able to regain linguistic functioning by recruiting new areas of the brain that were not typically central to speech contribution to play a key role in language.[1] Melzack et al. showed that human perception of pain is at least partially the result of past experience that causes the brain to rewire following painful stimuli.[2]

However, evidence in favor of neuroplasticity may seem contradictory in light of the argument that drugs have a long-term effect on the brain. After all, if the brain has the ability to change so much, doesn’t this mean that it will recover from any damage that is caused by drug use? Not necessarily. While the brain is able to recover from some degree of insult, the mechanism that causes drug users to experience a euphoric event is also involved in the long-term changes that result from such abuse. According to Uys and Reissner (Glutamatergic Neuroplasticity in Cocaine Addiction, Progress in Molecular Biology and Translational Science. Vol 98. 2011) despite the fact that initially, drugs such as cocaine activate the dopaminergic pleasure system, long term use of drugs causes the brain to recruit new areas to play a role in the mechanism. The authors state:

Over time and with chronic exposure, other structures involving glutamatergic and GABAergic transmission and the brain stress systems are subsequently recruited in latter stages of addiction. For example, key glutamatergic projections are sent from the [pre-frontal cortex], amygdala, and hippocampus, and GABAergic projections are sent from medium spiny neurons of the [nucleus accumbens] core and shell to the vental pallidum and back to the [ventral tegemental area] (371).  

This statement is central to the concept of addiction. Although the individual may enjoy the first time that he or she uses a given drug and may have a strong desire to use the substance again, the real consequences of addiction usually occur as a result of chronic use. This is at least partially due to the rewiring of the pleasure circuits in the brain. However, arguing that using drugs a single time is safe, given the fact that re-wiring cannot occur on the first exposure, is naïve. Although it may take a number of times to do irreparable remodeling of neurocircuitry, it seems clear that the long term changes that occur are not worth the pleasure that may result. Uys and Reissner offer support for this claim, stating, “Long-term potentiation is observed early in the VTA, following acute exposure to drugs of abuse. This LTP lasts at least 5 days following a single drug exposure” (373).

For more on neuroplasticity, see another post.

Great book on neuroplasticity.

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[1] Thompson, C. K. (2000). Neuroplasticity: Evidence from aphasia. J. Commun. Disord., 33, 357-366.

[2] Melzack, R., Coderre, T. J., Katz, J., & Vaccarino, A.L. (2001). Central neuroplasticity and pathological pain. Annals of the New York Academy of Sciences. 933, 157-174.