Our everyday life is often a series of habits played out under slightly different circumstances. The dictionary defines a habit as a regular tendency or practice that is hard to give up. In psychology, a habit is also an automatic reaction to a specific situation.
If you think about it - in many ways, habits are what make or break us. And it is with this realization that we try to cultivate certain habits over others - eating healthy, exercising, reading etc etc. Wouldn't it be nice if we understood how we can break a bad habit or form a good one? How long to repeat a task for it to become a habit or how long to avoid a task to break the habit? I would love to know how I can break my night-time dessert habit... ;) And I am sure you have a list of your own.
But scientifically - how much do we really know about habits, their formation and strengthening to optimize the process? Wouldn't it make life easier if we could easily throw out the bad habits like drinking and smoking and gain the good ones like exercising? What if you could control the obsessive habits of people suffering from obsessive compulsive disorders...? Wouldn't it all make life easy for so many people? Well, while psychologists have devoted a lot of attention to the aspect of our mind, very little was done from a neuroscience perspective because we lacked the necessary scientific tools. But a recent report on PNAS by Smith et al. tries to study habit formation and identifies salient principles.
Experience tells us that forming a habit requires repeated and durable representation of the movement and it involves a gradual transition from a flexible and goal directed behavior to a more fixed, habitual behavior. Classical studies using chemical inactivation and lesions of specific brain areas, identified the striatum as the brain area essential for the expression of habits. Such studies have also found a region in the median prefrontal cortex, called the infralimbic cortex (or ILC) in rodents to be essential for the expression of habits. This region of the brain, the ILC anatomically projects into sites that promote behavioral flexibility and this circuitry raises questions about how habits are controlled? The fact that habits take a long time to form (anywhere from 21 days to 66 days according to some psychology studies) favors a model where behaviors are gradually built and biased to automaticity. At the same time, the stability of a habit suggests that habits are being performed without constant biasing or higher order cortical control. The authors in this paper have tried to address some such fundamental questions about the nature and structure of a habit using optogenetics as a tool.
The authors introduce Halorhodopsin (eNpHR3.0), a light-driven ion pump specific for chloride ions found in ancient salt loving archaebacteria. Just as the blue-light activated channelorhodopsin which activates neurons and depolarizes them; halorhodopsin gets activated by yellow light and causes the silencing of resident cells by causing a chloride influx. The authors use a virally introduced form of halorhodopsin to inhibit the activity of select groups of neurons (glutamatergic pyramidal neurons) in the ILC and study their role in habit formation.
As an assay for habit formation, the authors use a T maze task and habituate/ train the rats to navigate this T maze. The rats are trained to run through a T-shaped maze in response to a cue and then to turn left or right depending on an auditory instruction, to receive one of two rewards in the form of chocolate milk or sucrose. For each rat, a reward was assigned to each arm of the T maze in response to the appropriate cue and entry into the incorrect arm resulted in no reward. the rats were trained repeatedly such that their peak performance accuracy was at ~90%. After this extensive training they de-valued one of the of the two rewards by mixing with a nauseating chemical and then tested in the maze experiments for habitual running to the arm now containing the devalued reward. Exposure to the tainted nauseating "reward" made the rats averse to it and then the rats were tested again in the maze (without any bait). If the animals again run to the devaluated reward as per the instruction, then they conclude that the behavior was habit driven than by active choice.
The experimental set up.
Over trained control rats (no halorhodopsin or no laser) behaved habitually in the maze and continued running to the devalued reward as per the instruction, as it was prior to the devaluation. This insensitivity clearly suggests that the training procedures produced ingrained, habitual maze runs. Now to test for the role of the ILC in this habit, the authors now perturb its activity during the run alone. After devaluation of the reward, the rats were subjected to a probe test where neither arm of the maze was baited but the auditory cues were provided. In this test, the ILC function was disrupted during the run and dramatically the rats behaved as though they had never acquired the habit in the first place. While the control rats kept running to the devalued goal according the auditory instruction, the rats without ILC function reduced their turns to the devalued arm, almost immediately (avg of 3 trials). This clearly suggests that the ILC was actively monitoring the expression of habitual behaviors, which appear to be ingrained and unsupervised.
Now, when the ILC activity was disrupted in the trained rats, they did not switch to inaction or random turning; instead, they continued to run to the other end arm which has the second reward or the non-devalued goal. These wrong-way turns were uninstructed and were not rewarded but their frequency still increased over days. This behavior suggested that the rats had actually developed a new habit of running to the non-devalued arm post the devaluation of their reward.
In order to test if the ILC plays the role of a on-off binary switch in the formation of a habit, the authors extended the laser mediated perturbation of the ILC after the probe test to different periods upto a month. When the ILC was disrupted for up to 6 days after the probe test, the rats showed to no detectable change in their behavior as both groups equally avoided the devalued reward arm. This suggests that the previous habit had been blocked and that the rats were now exhibiting outcome guided behavior. However, when the ILC was perturbed 2-3 weeks after the initial disruption, the effect was dramatic and surprising as the rats now suddenly reverted to their old behavior of running to the devalued arm when instructed. They also drank the devalued, nauseating reward every time they ran to it. This switch in the behavior was rapid and occurred within a few seconds. While control rats kept avoiding the devalued arm, the perturbation of the ILC led the rats to run to devalued arm and to regain their old habit. This kind of a temporal day-by-day analysis suggested that somewhere between 6 and 13 days, the old habit underwent a tipping point, where instead of being inhibited (as it was in days 1-6) it was suddenly promoted (as it was from day 13 onwards). This suggests that the ILC perturbation at day 13 might have resulted in blockade of the second habit thereby uncovering the original habit of running to the devalued arm. Thus, a new behavior takes around 6-13 days to become a habit and once it becomes a habit it becomes as susceptible as the old habit to any perturbation in the circuit.
Behavior when cued to the devalued goal for each rat and each trial showing control rats on day 6 post probe (PP6), and IL-halo rats the day before PP6 and on PP6.
These results clearly show that despite its seeming automaticity, habitual behaviors require online permission or supervision from the median prefrontal cortex. Further, from a learning and evolutionary perspective, in a competition between old habits and new, this prefrontal control appears to favor new habits if there is a competition between old and new habits. Fascinatingly, even as an ILC perturbation can also block an old habit, it can also abruptly bring back an old habitual behavior by blocking the newer one. The amazing thing though is that these manipulations in the medial prefrontal cortex affect the expression of the habitual behavior almost immediately.
One possible explanation for these observations is that while devaluation of the reward removes access of the original habit to the behavior circuit, its representation is nonetheless maintained in the brain and the delayed ILC perturbation unmasks it and makes it available/ dominant again. This interpretation is in accordance with earlier pavlovian conditioning studies where it was found that when a habit is broken, it is not forgotten, but just replaced by a new one. By this view the ILC would be regarded an online executive controller favoring newer habits over the older ones.
These findings do a lot to clarify our existing understanding of habits as automatic, outcome independent, non-cognitive actions to being under the constant purview of the prefrontal cortex for any contingencies or unexpected behaviors. While these results suggest that old behaviors are only masked by newer ones, they do not answer how behaviors become latent or how they are unmasked. The coordination between the different cortical areas of the brain in making these choices is also unknown.
These findings could be potentially useful to tackling problematic behaviors, addictions and other obsessive habits which are seen in major neurologic and neuropsychiatric disorders. Being able to spur robust and rapid behavioral change by targeting the ILC could be a valuable tool in many clinical settings in addition to being a personal asset.
Imagine how much better the world would be if you didn't crave for that last piece of cheesecake or succumb to the temptation of yet another cup of coffee... ;)
And now you can probably appreciate the old proverb - "old habits die hard" - because they do not really die...
References:
If you think about it - in many ways, habits are what make or break us. And it is with this realization that we try to cultivate certain habits over others - eating healthy, exercising, reading etc etc. Wouldn't it be nice if we understood how we can break a bad habit or form a good one? How long to repeat a task for it to become a habit or how long to avoid a task to break the habit? I would love to know how I can break my night-time dessert habit... ;) And I am sure you have a list of your own.
But scientifically - how much do we really know about habits, their formation and strengthening to optimize the process? Wouldn't it make life easier if we could easily throw out the bad habits like drinking and smoking and gain the good ones like exercising? What if you could control the obsessive habits of people suffering from obsessive compulsive disorders...? Wouldn't it all make life easy for so many people? Well, while psychologists have devoted a lot of attention to the aspect of our mind, very little was done from a neuroscience perspective because we lacked the necessary scientific tools. But a recent report on PNAS by Smith et al. tries to study habit formation and identifies salient principles.
Experience tells us that forming a habit requires repeated and durable representation of the movement and it involves a gradual transition from a flexible and goal directed behavior to a more fixed, habitual behavior. Classical studies using chemical inactivation and lesions of specific brain areas, identified the striatum as the brain area essential for the expression of habits. Such studies have also found a region in the median prefrontal cortex, called the infralimbic cortex (or ILC) in rodents to be essential for the expression of habits. This region of the brain, the ILC anatomically projects into sites that promote behavioral flexibility and this circuitry raises questions about how habits are controlled? The fact that habits take a long time to form (anywhere from 21 days to 66 days according to some psychology studies) favors a model where behaviors are gradually built and biased to automaticity. At the same time, the stability of a habit suggests that habits are being performed without constant biasing or higher order cortical control. The authors in this paper have tried to address some such fundamental questions about the nature and structure of a habit using optogenetics as a tool.
The authors introduce Halorhodopsin (eNpHR3.0), a light-driven ion pump specific for chloride ions found in ancient salt loving archaebacteria. Just as the blue-light activated channelorhodopsin which activates neurons and depolarizes them; halorhodopsin gets activated by yellow light and causes the silencing of resident cells by causing a chloride influx. The authors use a virally introduced form of halorhodopsin to inhibit the activity of select groups of neurons (glutamatergic pyramidal neurons) in the ILC and study their role in habit formation.
As an assay for habit formation, the authors use a T maze task and habituate/ train the rats to navigate this T maze. The rats are trained to run through a T-shaped maze in response to a cue and then to turn left or right depending on an auditory instruction, to receive one of two rewards in the form of chocolate milk or sucrose. For each rat, a reward was assigned to each arm of the T maze in response to the appropriate cue and entry into the incorrect arm resulted in no reward. the rats were trained repeatedly such that their peak performance accuracy was at ~90%. After this extensive training they de-valued one of the of the two rewards by mixing with a nauseating chemical and then tested in the maze experiments for habitual running to the arm now containing the devalued reward. Exposure to the tainted nauseating "reward" made the rats averse to it and then the rats were tested again in the maze (without any bait). If the animals again run to the devaluated reward as per the instruction, then they conclude that the behavior was habit driven than by active choice.
The experimental set up.
Over trained control rats (no halorhodopsin or no laser) behaved habitually in the maze and continued running to the devalued reward as per the instruction, as it was prior to the devaluation. This insensitivity clearly suggests that the training procedures produced ingrained, habitual maze runs. Now to test for the role of the ILC in this habit, the authors now perturb its activity during the run alone. After devaluation of the reward, the rats were subjected to a probe test where neither arm of the maze was baited but the auditory cues were provided. In this test, the ILC function was disrupted during the run and dramatically the rats behaved as though they had never acquired the habit in the first place. While the control rats kept running to the devalued goal according the auditory instruction, the rats without ILC function reduced their turns to the devalued arm, almost immediately (avg of 3 trials). This clearly suggests that the ILC was actively monitoring the expression of habitual behaviors, which appear to be ingrained and unsupervised.
Now, when the ILC activity was disrupted in the trained rats, they did not switch to inaction or random turning; instead, they continued to run to the other end arm which has the second reward or the non-devalued goal. These wrong-way turns were uninstructed and were not rewarded but their frequency still increased over days. This behavior suggested that the rats had actually developed a new habit of running to the non-devalued arm post the devaluation of their reward.
Behavior when cued to the devalued goal for each rat and each trial showing control rats on day 6 post probe (PP6), and IL-halo rats the day before PP6 and on PP6.
These results clearly show that despite its seeming automaticity, habitual behaviors require online permission or supervision from the median prefrontal cortex. Further, from a learning and evolutionary perspective, in a competition between old habits and new, this prefrontal control appears to favor new habits if there is a competition between old and new habits. Fascinatingly, even as an ILC perturbation can also block an old habit, it can also abruptly bring back an old habitual behavior by blocking the newer one. The amazing thing though is that these manipulations in the medial prefrontal cortex affect the expression of the habitual behavior almost immediately.
One possible explanation for these observations is that while devaluation of the reward removes access of the original habit to the behavior circuit, its representation is nonetheless maintained in the brain and the delayed ILC perturbation unmasks it and makes it available/ dominant again. This interpretation is in accordance with earlier pavlovian conditioning studies where it was found that when a habit is broken, it is not forgotten, but just replaced by a new one. By this view the ILC would be regarded an online executive controller favoring newer habits over the older ones.
These findings do a lot to clarify our existing understanding of habits as automatic, outcome independent, non-cognitive actions to being under the constant purview of the prefrontal cortex for any contingencies or unexpected behaviors. While these results suggest that old behaviors are only masked by newer ones, they do not answer how behaviors become latent or how they are unmasked. The coordination between the different cortical areas of the brain in making these choices is also unknown.
These findings could be potentially useful to tackling problematic behaviors, addictions and other obsessive habits which are seen in major neurologic and neuropsychiatric disorders. Being able to spur robust and rapid behavioral change by targeting the ILC could be a valuable tool in many clinical settings in addition to being a personal asset.
Imagine how much better the world would be if you didn't crave for that last piece of cheesecake or succumb to the temptation of yet another cup of coffee... ;)
And now you can probably appreciate the old proverb - "old habits die hard" - because they do not really die...
References:
1) Reversible online control of habitual behavior by optogenetic perturbation of medial prefrontal cortex
Kyle S. Smith, Arti Virkuda, Karl Deisserothb, and Ann M. Graybiel
Contributed by Ann M. Graybiel, September 18, 2012 (sent for review August 20, 2012) PAS, November 2012
