by Ben Taub
Bad habits are never easy to kick, and the reason could be down to more than just flimsy will power. According to a new study into the neurological mechanisms behind habit formation, such problematic modes of behavior can actually cause changes in the way the brain is wired, to the point where our little (or not so little) imperfections become written into our mental machinery.
This process is mediated via the dorsolateral striatum, a brain region that processes sensory-motor signals in order to stimulate the striatal projection neurons (SPNs) of another part of the brain called the basal ganglia, which has been associated with controlling habitual behavior. The SPNs in the basal ganglia are arranged in two pathways, called the direct and indirect pathways.
Previous research has indicated that the SPNs of the direct pathway stimulate action, while those of the indirect pathway inhibit action. As such, the direct and indirect pathways are sometimes described as the “go” and “stop” pathways, respectively.
To test how these mechanisms become disrupted by the formation of habits, a team of researchers from Duke University conducted an experiment in which mice were trained to press a lever in order to receive a sugary pellet. When the supply of these treats was later stopped, some mice continued to press the lever – indicating they had formed a habit – while others did not. The researchers then used a dye to observe the firing of neurons in the basal ganglia of the mice, noting the differences between those who had formed a habit and those who had not.
Describing their findings in the journal Neuron, the study authors reveal that firing rates increased for both the direct and indirect pathways in habit-forming mice, and that the order in which these neurons fired had become disrupted. More specifically, they found that the SNPs of the “go” pathway tended to fire earlier than those of the “stop” pathway, which would appear to explain why the mice habitually performed a particular action.
Furthermore, they noted that this disparity between direct and indirect SNPs was apparent throughout the basal ganglia, rather than just in those neurons involved in the lever-pressing task. Because of this, they suggest that the formation of a single habit causes “broad modifications” to the neural firing pathways of the brain, which may then make a person more vulnerable to developing other habits. In other words, it may be possible to develop a “habit-forming brain.”
To conclude their study, the researchers attempted to erase the habit that some of the mice had developed. To do so, they began rewarding mice with treats if they stopped pressing the lever, and then once again traced the neural patterns in those who overcame their habit.
This was found to result in a reduction in direct SNP firing, but did not affect indirect SNP firing. Therefore, the study authors conclude that while the formation of a habit distorts both pathways, the erasure of this behavior only affects one of the two pathways.
Whether or not this research can be used to develop new treatments for those with harmful habits such as addictions remains to be seen. For instance, while these findings raise the possibility of erasing habits by stimulating certain neurons, such as through a technique known as transcranial magnetic stimulation, the side effects of any such intervention could ultimately outweigh the benefits, since the neurons of the basal ganglia are involved in a wide range of processes beyond those associated with habit formation.