NRSC 2110 Blog

Last week I returned home from running some errands to find my husband on his laptop playing an action packed video game while the kids are sitting on the floor playing games on the Wii. I want to let them relax but I'm worried they are all killing brain cells with these mindless games.

Maybe, I worry too much? The article Children Wired: For Better or Worse found in the September 9, 2010 issue of Neuron magazine describes some benefits to playing action-packed video games. This is good because in this highly technological world we live in I'd be fighting a losing battle in my home.

Games that showed the highest benefits were full of action and were multidimensional. These games also pull the player in emotionally. It is important to note that studies were conducted with a young adults and not children because of the violence in some of the video games. Some enhancements have been found in vision, attention, cognition, and motor control. The medical community and healthcare professionals are seeing benefits in gaming for patients also. Some research being done shows people with amblyopia (a developmental deficit of vision) and those with attention issues are benefitting from playing video games.

For the younger kids, preschool programming showed some cognitive benefits, in particular an increase in the vocabulary of preschoolers when they view shows like Dora the Explorer. For obvious reasons shows like Teletubies actually prove to reduce language skills. Preschool programs that elicit responses, labels objects, and models proper language in addition to modeling social skills benefit children. However, the new baby/infant videos do not seem to have the same types of benefits. Babies benefit from watching their parents interact in the world. This is not something that can be gained from a video or TV show.

It may be that there is a link in the social skills being taught in preschool programming and the high intensity emotional component of action packed video games that leads to the cognitive benefits that are being observed in these studies. Educational computer games incorporate repetition and interaction as a way of teaching "educational" information but do not have an emotional component. Therefore educational computer programs do not seem to have the same benefits as the emotionally charged video games.

Until now the world of education and the world of behavioral science has studied technology. PET scans and fMRI are allowing neuroscience to share in this new area of research. These new brain-imaging techniques are allowing for real time studies of the brain. This is beneficial to studying the effects gaming has on the brain. Studies are finding that video games are affecting reward pathways. Neuroscience will be able to shed light on the effects these games are having on executive function and control of attention, as well as, reward pathways. Hopefully new studies will emerge that will incorporate neuroscience and technology so educational programs can be developed that will illicit the same learning benefits as action packed video. Wouldn't it be cool if learning history and math on the computer were just as fun (and beneficial) as playing one of those action packed video games?!

I?m sure most of us can remember reaching a certain age in high school and having our parents wish we spent more time learning our school material than learning bad habits (such as smoking) from our peers. The irony? The same potentiation that seems to be responsible for the learning and memory that allows us to master our scholastic material may be responsible for our ?learned? addictions. (And our parents thought they could blame the bad kid down the street).

A study (http://www.cell.com/neuron/abstract/S0896-6273%2809%2900580-7) published in the September 2009 issue of Neuron indicates that Dopamine (DA) may be what helps enable our synapses to undergo the types of synaptic plasticity that underlies our addictions and appears to have many similarities to the plasticity underlying our learning and memory including a strong involvement of the hippocampus.

It has been established that both DA signaling and the hippocampal circuitry have a major role in drug addiction. The researchers in this study aimed to study the in vivo synaptic potentiation underlying addiction in awake freely moving animals. Nicotine had already been shown to alter synaptic plasticity, however it had been done in animals that were either anesthetized using an agent that is known to alter the functionality of ligand-gated channels, or given enough nicotine to give an awake mouse a seizure. The researchers here introduce a more physiologically relevant measurement.

In their study, the researchers used the amplitude of the pop spike (PS) (the spike that is produced when a population of cells all fire together) to measure potentiation of synaptic transmission. With the recording electrode placed in the dentate gyrus, they found that when they injected nicotine into mice the PS amplitude showed a significant increase over the baseline animals that were not given nicotine; this indicates that significant synaptic potentiation was induced by nicotine exposure.

Having first established that the nicotine was acting through nicotinic acetylcholine receptors, they injected nicotine directly into the hippocampus. Finding that the nicotine now did not induce a significant change in synaptic potentiation, their results suggest that nicotine must exert its effects in a way that extends beyond the hippocampal circuitry alone.

So where does dopamine fit in to our learned addiction? Well without dopamine our potentiation disappears. When researchers injected a D1-type DA receptor antagonist (both systemically and locally into the hippocampus) the potentiation induced in the hippocampal circuitry by nicotine is inhibited. This strongly suggests that the D1 DA receptors enable the nicotine induced synaptic potentiation. Also of interest, using an agonist of the D2-type DA receptors (these are autoreceptors that will inhibit the firing of midbrain DA delivering neurons when activated) inhibits the nicotine-induced potentiation. However, when an antagonist of the D2-type receptors is used, allowing an even larger DA signal to be delivered from the midbrain, we see enhanced potentiation even beyond the before seen nicotine-induced potentiation. This suggests the magnitude of the DA signal influences the strength of the nicotine-induced potentiation.

How does this translate into memory based behavioral observations? The conditioned place preference (CPP) test was used to find out. When nicotine was administered significant CPP was observed. So it appears they are learning an addiction.

So the next time you see all the college undergrads smoking on their breaks between courses you can appreciate the irony in that the very same synaptic mechanisms allowing them to master their studies allowed them to learn their addiction that interferes with said studies. With the help of DA of course.