Understanding the Brain’s Plasticity

Posted: June 7, 2010 at 1:01 am, Last Updated: September 8, 2011 at 1:18 pm

By Colleen Kearney Rich

Kim Avrama Blackwell. Photo by Evan Cantwell

Mason neuroscientist Kim Avrama Blackwell has the best of two worlds, working in both “wet” and “dry” labs as the principal investigator of the Computational and Experimental Neuroplasticity Laboratory at the Krasnow Institute for Advanced Study.

A wet lab is what one usually thinks of when picturing a laboratory. It has test tubes, Petri dishes, microscopes and researchers doing biological or chemical experimentation.

A dry lab refers to in silico science and laboratories where computer-generated models are used for computational analysis.

Blackwell, who has been internationally recognized for her work with computer models, brings diverging expertise and degrees in veterinary medicine and bioengineering to her work.

“To be a good neuroscientist, you need to know a lot about life sciences,” Blackwell says. “That part I learned in veterinary medicine. Most mammals are very similar, particularly the basic mechanisms of how our brains work.”

Blackwell’s area of expertise is neuroplasticity, an area of science that focuses on learning and the brain’s ability to make connections.

“We tend to think of learning as an experience-dependent, long-lasting change in behavior, but learning on the whole animal level must be tied to consistent changes on the cellular level. In other words, my experience is translated into inputs to my neurons.”

Blackwell offers up Pavlov’s dog as an example. Widely known for describing the phenomenon of classical conditioning, Pavlov was able to elicit a reflex response, salivating, from dogs by providing them with certain cues.

“Changes in auditory neurons and taste neurons occurred repeatedly,” Blackwell says, putting the experiment in neurological terms.

“So repeated presentation of synaptic inputs produces long-lasting changes in the neuron’s behavior. I’m studying changes in neuron behavior because I believe those changes in neurons can in turn produce long-lasting changes in behavior.”

Another way of explaining this neural reaction is to look at addiction.

“Addiction has a strong learning component,” she says. “When an addict goes into the same environment in which they used drugs, it can stimulate a craving. The sights, the smells and the sounds are all triggers. So you have to remove addicts from that environment. That’s why it is difficult to change that behavior.”

To learn about the brain’s plasticity, Blackwell focuses on the basal ganglia, the part of the brain linked to learning and motor function, and the neurotransmitter dopamine.

“I’m studying how dopamine produces plasticity,” she says. “When you get a reward, your dopamine neurons fire. When you see something novel, your dopamine neurons fire.

“One of the things we know is that, in a part of the basal ganglia, if you remove the dopamine, you don’t see that experience-dependent plasticity.”

A part of Blackwell’s research focuses on Parkinson’s disease. Photo by Evan Cantwell

A part of Blackwell’s research focuses on Parkinson’s disease. For those affected by Parkinson’s, the dopamine receptors in the brain are destroyed.

Current therapies involve replacing the dopamine, but this treatment only provides relief for a short time. Blackwell believes the solution to Parkinson’s may lie farther down the neural pathway.

“When dopamine binds with its receptors, many other molecules get activated. A whole cascade of biochemical reactions takes place,” Blackwell says. “If the dopamine structure is impaired, you aren’t going to learn as well.”

This is complicated by the fact that the part of the brain that receives the dopamine input is the part coordinating complex movement.

“When the dopamine goes away, we see this motor deficit. We aren’t sure how that is connected to learning, but it is somehow related.”

Blackwell is using computer modeling and lab experiments in her research on this pathway.

“Some of the molecules ‘downstream’ from dopamine are critical to dopamine’s function. I want to find out which of those molecules are critical and how things change when you block those molecules. We have to understand what those molecules are and how they change the activity of the neuron.”

Blackwell believes that when those molecules are identified they could be targets for drug design, and one day medicine could bypass dopamine altogether in the treatment of Parkinson’s.

This article appeared in a slightly different form in Mason Research 2010.

Write to mediarel at gazette@gmu.edu