Recently, an international team of researchers reported that the cerebellum may play a previously unforeseen role in brain alterations associated with the addictive consumption of drugs. Until now, the cerebellum—which has historically been viewed by most neuroscientists as primarily the seat of fine-tuned motor control and coordination—has gone under the radar of drug addiction specialists.
The latest reports linking the cerebellum and drug addiction were based on a broad range of groundbreaking research published over the past two years. These findings were recently compiled and featured in two different journals: Neuroscience & Biobehavioral Reviews and the Journal of Neuroscience.
Bringing all of this research together was the brainchild of Marta Miquel, professor in the research group Addiction and Neuroplasticity at the Universitat Jaume I (UJI) in Spain.
Miguel spearheaded her own original research as well as the initiative to collect multidisciplinary research from a broad spectrum of international institutions and to present these cerebellar findings cohesively under one umbrella. (Cerebellar is the sister word to cerebral and means “relating to or located in the cerebellum.”)
In addition to the UJI team, contributing research for this compilation of studies on the cerebellum and addiction came from the University of Cambridge and University of Leeds (United Kingdom); University of Turin (Italy); Universidad Veracruzana (Mexico); the University of Kentucky, Washington State University, and McLean Hospital Translational Neuroscience Laboratory and Mailman Research Center (USA).
In describing the objective of the first review, “Have we been ignoring the elephant in the room? Seven arguments for considering the cerebellum as part of addiction circuitry,“ the scientists describe their mission stating,
“Our goal is not to review animal and human studies exhaustively but to support the inclusion of cerebellar alterations as a part of the physiopathology of addiction disorder.”
The following bullet points were included in the aforementioned Neuroscience & Biobehavioral Reviews report that presents seven arguments for considering the cerebellum as part of addiction circuitry:
In the past decade, countless studies have corroborated empirical evidence that specific brain regions—including the basal ganglia, prefrontal cortex, amygdala, and hippocampus—play a role in the neural circuitry that drives addictive behavior.
However, as I mentioned earlier, the cerebellum has not been considered a part of the brain circuitry of addictive behaviors until very recently because it was considered by most neuroscientists to be a subcortical brain structure exclusively dedicated to motor control and motor coordination.
My father, Richard Bergland, was a neuroscientist, neurosurgeon, and author of The Fabric of Mind (Viking). In the late-twentieth century, my dad became intrigued by the disproportionate number of neurons in the "non-thinking" cerebellum when compared to the cerebrum (Latin for "brain") and cerebral cortex, which most people consider the "thinking cap."
The cerebellum is only 10 percent of brain volume but houses roughly 80 percent of your brain's total neurons. My dad would often spur on the curiosity of his colleagues and encourage them to be more proactive about investigating the enigmatic riddles and hidden powers of the cerebellum by constantly saying, "We don't know exactly what the cerebellum is doing. But whatever it's doing, it's doing a lot of it."
As a brain surgeon, my dad was able to observe specific cognitive and behavioral changes in his neurosurgery patients who had cerebellar damage to microzones within the cerebellum. Before, during, and after an operation, he could witness firsthand how cerebellar damage or dysfunction often extended far beyond simply fine-tuned motor control.
Decades ago, my dad became convinced that the cerebellum was more than just the seat of muscle memory and coordination. Unfortunately, as a neuroscientist, he was unable to prove his neurosurgery-based hypotheses about the cerebellum empirically in a scientific laboratory during his lifetime. When my father died in 2007, I made a vow that I would keep my antennae up for all the latest research on the cerebellum and do my best to communicate future findings to a general audience, as I am doing now.
In a February 2017 statement to UJI that echoes my father's sentiments about the cerebellum, Marta Miquel described her intrigue with the link between the cerebellum and drug addiction as being rooted in the cerebellum's uncanny distribution of neurons. Miguel said,
"The cerebellum comprises 80 percent of all neurons in the brain; Contains 60 billion neurons packaged in only 10 percent of brain mass and is a fundamental structure in the consolidation and automation of learned behavioral repertoires."
The latest analysis suggests that much more cerebellar research is necessary to better understand the brain mechanisms that drive drug addiction. Future cerebellar discoveries could result in more effective treatments for drug addiction.
The sooner neuroscientists are able to unravel the many mysteries of the cerebellum, the more quickly we can develop and implement fresh approaches for treating addiction and substance abuse.
The cerebellum has been overshadowed by the cerebrum for too long. Stay tuned for upcoming research that will undoubtedly give the cerebellum top billing and put the previously underestimated "little brain" on center stage and in the spotlight it deserves.
Marta Miquel, Dolores Vazquez-Sanroman, María Carbo-Gas, Isis Gil-Miravet, Carla Sanchis-Segura, Daniela Carulli, Jorge Manzo, Genaro A. Coria-Avila. Have we been ignoring the elephant in the room? Seven arguments for considering the cerebellum as part of addiction circuitry. Neuroscience & Biobehavioral Reviews, 2016; 60: 1 DOI: 10.1016/j.neubiorev.2015.11.005
Barbara A. Sorg, Sabina Berretta, Jordan M. Blacktop, James W. Fawcett, Hiroshi Kitagawa, Jessica C.F. Kwok, Marta Miquel. Casting a Wide Net: Role of Perineuronal Nets in Neural Plasticity. The Journal of Neuroscience, 2016; 36 (45): 11459 DOI: 10.1523/JNEUROSCI.2351-16.2016
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