Smart phone use changes the brain

One of the most remarkable things about our brains is how organized they are. Sensory information from our eyes, mouth, skin, nose and ears goes to different locations in the brain. For example, visual signals are processed first in the very back of the brain, whereas sensations of touch and pain activate the middle region of the brain called the somatosensory cortex.

Functional organization of brain cortex. (Source: imgarcade.com/1/sensorycortex)

Remarkably, the brain gets even more organized from there. Within the visual cortex, there are columns of neurons that only respond to light that is horizontal and others that only respond to lines that are tilted 45 degrees. The somatosensory cortex is also highly organized, with different parts of the body represented by specific sets of neurons. If you were to send electrical shocks into one specific area of the somatosensory cortex to activate those neurons, you may elicit feelings of touch from the right thumb, even though the subject is not being touched at all. Move those electrical signals over slightly to another area, and the subject may feel touch instead coming from the palm of their hand.

Wow, right? But here’s the real mind blower: this organization can change over time as the person experiences different sensory inputs. If you are a violin player, you feel the strings with your fingertips a lot, so the fingertip part of the somatosensory cortex is super active. This extra activity allows the fingertip representation in the brain to grow and recruit nearby neurons to also respond to touch in the fingertips. The cortical representations are “plastic” and always changing with use.

A violin player may practice this one particular skill a lot, but what about other activities we do everyday with less intensity, like using smart phones? Think about how often you are swiping the screen with your thumb. That’s a lot of sensory information being sent to the thumb part of your somatosensory cortex. Would this increase the thumb representation in your brain? A recent paper by Gindrat et al. addressed this exact question using EEG to record brain activity in smart phone users versus people with the old-style cell phones.

Electroencephalography

How can you actually measure the area of body representations in the somatosensory cortex? You could stick electrodes into people’s brains and record the activity in their neurons, but that’s a little invasive. You could put them into a MRI machine and measure brain activity when you touch their thumbs, but that is time consuming for so many subjects (37 total). Instead, the authors used a method known as electroencephalography, or EEG, which consists of 62 surface electrodes placed on the scalps of the subjects. Each electrode records the summed electrical activity from all the neurons positioned right under the electrode. Before an experiment, all the electrodes would be picking up a baseline of activity from lots of different neurons firing asynchronously. However, during an experiment, there is a single stimulus (like touching the subject’s thumb), which elicits activity in a lot of neurons all at the same time. This activity summates to give one large response called the event related potential (ERP), which is recorded by the nearest electrodes.

EEG electrodes record brain activity (source: Wikimedia commons)

Finger representations in smart phone users

The ERPs for the thumb, index finger and middle finger were larger for the smart phone users than for the non-touchscreen users. There was a correlation between the amount of phone use per hour and the ERP, so the more use, the greater the ERP, which is to say the more activity in the somatosensory cortex. The number of electrodes recording the ERP was greater in the touchscreen users, so when you touch the thumb of a touchscreen user, a larger part of the somatosensory cortex responds. In other words, the thumb representation was larger in smartphone users who use their thumbs more often.

The more recently the subjects had used their phones intensely, the larger the ERP for the thumb, which indicates that brain remodeling occurs on a very short time scale (within 10 days in this experiment). Interestingly, there was no correlation between ERPs and the age at which the subject started using a touchscreen. This is in contrast to the previous experiments done with trained violin players, which did show a correlation between the size of the finger representations and the age at which they first started playing. The authors suspect that a trained violinist develops a more stable sensory representation than touchscreen users who are casually using their phones (as opposed to years of disciplined practice).

So the take-home message is that normal day-to-day activities can influence brain plasticity and the way our sensory representations are organized in our brains. This could be a good thing, because subjects develop better touchscreen skills. On the other hand, the enlarged thumb representation could cause focal dystonia, which is characterized by involuntary muscle contractions and sometimes pain, as the various body part representations lose their distinct boundaries and start to overlap. This probably won’t be a problem for most phone users, but be forewarned all you smart phone addicts out there.

Isolation and drug addiction

We all know that adverse, early life experiences can affect normal development and the ability to lead a happy and healthy adult life.  A number of recent studies have shown that rodents which are mistreated as pups have long lasting changes to their gene expression (i.e. epigenetics).  They are more anxious and have a harder time forming new memories.  A paper this week in Neuron builds upon these results, by studying the effects of social isolation on the “reward pathway” in the brain.

Reward pathway

What is a reward pathway?  Deep in the brain is a region known as the ventral tegmental area (VTA), which makes connections to the nucleus accumbens and prefrontal cortex.  When we do something that is naturally good, like eating or sex, the neurons in the VTA release dopamine onto the nucleus accumbens and we interpret that as “feeling good”.  This is our reward for doing something that will help us survive and procreate. 

The Reward Pathway in a brain cross section (from brainfacts.org)

Many drugs of abuse like cocaine, amphetamines and alcohol increase the amount of dopamine signaling in this pathway; this is one reason why drugs produce a “high”.  When this pathway gets overstimulated by increased drug use, the brain will try to compensate by making the pathway less efficient.  This is why drug users feel depressed when not on drugs and why higher and higher concentrations of drugs are necessary to produce the same high feeling.  This is a neurological explanation for drug addiction.  Drug abusers also start to make connections in their lives, and in their brains, between environments (a certain room, certain people, etc) and the feeling of reward.  Getting sober is so difficult because the brain has to unlearn these connections and the reward system has to recover back to its normal level of activity.

Plasticity

Before we talk about the paper, I need to introduce one more concept.  Neurons become activated when channels in their membranes open and positive ions rush in.  They can then pass on this signal to another neuron by releasing neurotransmitters (like dopamine) onto the next neuron.  The activity in the neuron and the amount of transmitter it releases into the synapse can change over time, based on that neuron’s previous experiences.  This is known as synaptic plasticity.  There are short-term changes, like facilitation, and longer-term changes (we’re talking hours and days here).  One of the more famous types of long-term plasticity is called long term potentiation (LTP) and is thought to underlie learning and memory.  When drug users start to become addicted, these types of long term changes to neuronal activity are occurring throughout the reward pathway.

Social isolation and VTA neurons

The experiment begins when young male rats were either housed together in groups of 3 or alone.  The researchers then recorded neuronal activity of VTA neurons under various conditions.  They found that rats that were isolated for more than 3 weeks, specifically during the equivalent of the rats’ early adolescence, can more easily induce LTP in the VTA neurons.  In other words, rats that had no social interactions during a critical period had more sensitive VTA neurons.  That is to say, their reward pathway is primed to be overstimulated, just like during repeated drug use.

What are the behavioral manifestations of having a sensitive reward pathway?

The next set of experiments they did is called conditioned place preference.  The rats were placed in a cage that had two different compartments, with different wall colors and floor textures.  The rats were then injected with amphetamine in one of those particular compartments, so they learned to associate the drug high with that environment.  The rats were then given a choice between the two compartments and inevitably they went to the room that was associated with the drug.  The researchers found that isolated rats had a greater preference for the drug room and developed the preference sooner than the control rats.  Social isolation as an adolescent causes an increased rate of learning an association between drugs and environment.  This could make these rats more vulnerable to drug addiction. 

What about unlearning the drug association?

After the drug testing, the rats were exposed repeatedly to the drug room, but this time they didn’t receive any drugs.  This is called extinction of a memory and it is measured by the rats losing their preference for the former drug compartment.   Socially isolated animals had a significantly slower rate of unlearning the preference.  Their memory was more resistant to extinction.  If their VTA neurons are overly sensitive, then it may be harder to rewrite that connection in the brain between environment and reward.

In the context of drug addiction, these findings are big.  An adverse early adolescence can prime the brain to develop addiction more easily and make it harder to sober up.  If the VTA neurons start firing every time you go through an environment associated with drugs, you’re going to want to take a hit again.  The authors bring up an interesting point that social isolation generally causes a depression of neuronal activity in places like the hippocampus (the site of learning), so maybe the increased activity in the VTA is the way for the brain to maintain some sort of homeostasis – some areas increase, some decrease, but overall the brain may have normal amounts of activity.  This is an interesting way of looking at this problem.  I suspect that social isolation offers little in the way of rewards, so the reward pathway is trying to compensate by getting more sensitive.  It will be interesting to see if there is also a connection with changes in gene expression.  The authors explain how the VTA neurons get overactive, from a cellular point of view, but what actually initiates those changes?  And how can social interactions feed into the biology of the cell? 

Plastic axonal trees

You can’t teach an old dog new tricks…or can you?

We’ve all heard about how the brain slows down as we age.  We’re constantly losing brain cells.  Neurons become “static” and cannot make new connections.  Is this true?  Are we really doomed to a lifetime of deteriorating mental function?

A paper by Oberlaender et al came out this week in the journal Neuron that disputes this common view of the adult brain.  They studied plasticity in the adult rat somatosensory cortex.  Plasticity refers to the ability of neurons to change shape, connections and activity levels in response to environmental changes.  The somatosensory cortex is the area of the brain that processes touch sensation.  In the rat (and mouse), the somatosensory cortex is organized into barrels, where each cylindrical chunk of brain responds only to signals sent from an individual whisker.  The sensory nerves in a whisker travel to the brainstem first, then they make a stop in the thalamus (a deep region of the brain), and finally the thalamic neurons synapse with cortical neurons in layer 4 (remember that the brain cortex is arranged into 6 layers). 

The somatosensory circuitry, from a sensory neuron (pink) 
to the brainstem (medulla) to the thalamus and then somatosensory cortex.

It has been shown before in the adult rat somatosensory cortex that the neurons can undergo structural and functional changes in response to changes in activity.  This kind of plasticity has only been observed before in the cortex; other areas of the brain were thought to be static once the brain reaches the adult stage.  Oberlaender et al. show, however, that the neurons from the thalamus can also undergo structural changes in the adult brain.

Changes in axonal morphology

To induce neuronal plasticity, the researchers trimmed a single whisker on a group of rats.  This is a painless procedure, so they don’t have to take into account responses due to an injury.  This trimmed whisker will no longer be sensing the environment, so its sensory neurons will be silent.  Three days later they filled the thalamic neurons associated with that whisker with a dye, so they could image the shape of the neurons. 

We need to take a brief pause here to discuss neuronal anatomy: Neurons have a round cell body, dendrites which receive signals from other neurons and axons which send signals to other cells.  Axons can travel great distances and make synapses with many different cells.  The general consensus in the field is that as we learn something new, more synapses and connections are made between neurons.  The image below is a thalamocortical rat neuron (a thalamic cell that makes synapses with the cortex).  You can really see that the axon and dendrites have lots of branches and each of those branches may have multiple synapses to other neurons.  This is why neurons are often compared to trees with their branching limbs.

Thalamocortical neuron.  From Destexhe et al., 1998, J. Neuro.

The authors compared the morphology of thalamic neurons from control rats to those that had their whisker trimmed.  The neurons corresponding to the  trimmed whiskers had considerably shorter and less branched axons.  Remember, these neurons in the thalamus are no longer receiving signals from the whisker, and in just three days they started to retract.  This often happens in the cortex, where an unused area of the brain will just shrink up or get taken over by other neurons.  This is the first time this has been shown for a non-cortical region of the brain. 

Functional compensation

The shortened axons are obviously making fewer synapses with cortical neurons, so these neurons should be less active.  However, when they recorded electrical activity, there was no difference in L4 cortical cells in the trimmed mice compared to controls.  The authors investigated this more thoroughly and looked at synchrony between cells.  Neurons that are active at the same time will often add up their signals at the next connection, so this is another way of looking at activity in the brain.  The trimmed mice had more synchronous cortical cells than the controls.  That makes no sense, right?  They have fewer synapses, so how could they be more synchronized?  Apparently there must be some form of compensation for the decrease in axon length and synaptic connections.  In other words, the remaining synapses become stronger to maintain a normal level of electrical activity.  We call this process homeostasis, which happens at many different levels in our bodies (temperature regulation, blood sugar, etc).

To summarize, trimming the whiskers results in less signaling to the whisker area of the thalamus.  As a result, the thalamic neurons become shorter and less branched.  They make fewer synapses onto the cortex, but it doesn’t matter because these synapses increase their strength to maintain a physiological activity level. 

The important point here is that adult neurons can undergo structural plasticity (shorter axons) and functional plasticity (strengthening of synapses) as a result of experience (or lack thereof).  These changes happened really quickly – only three rat days.  The authors conclude that “thalamocortical input to cortex remains plastic in adulthood, raising the possibility that the axons of other subcortical structures might also remain in flux throughout life.”  There’s hope for us after all!

This blog title was somewhat inspired by the Radiohead song "Fake Plastic Trees".  Oh the 90's.