Wanting vs liking

I’m fascinated by the processes that inform and drive addiction to substances and behaviours.  The nurse  and psychology graduate in me just loves this stuff and I love to share it because if we can understand it better it gives us more tools to tackle it.  So in the first of two posts I’m going to look at incentive sensitization and then kindling or more simply ‘wanting vs liking’.

wanting vs liking
wanting vs liking

I found an excellent article on the PLOS blog looking at the development of addiction.  This is what they said:

Sometimes, while daydreaming in the shower or in the car, an insight hits you out of the blue. That happened last week. It occurred to me that the best neurobiological model of addiction has a serious missing link. Addiction develops. It grows. A successful theory of addiction needs to be a developmental theory – a theory of neural development.

In my view, the neural basis of addiction is best captured by Berridge and Robinson’s model of incentive sensitization. In a nutshell, these researchers show that “wanting” and “liking” are quite independent, subserved by different neurochemicals, and addiction is characterized by “wanting,” not “liking.” That helps explain why addicts keep on craving – and obtaining – their substance of choice long after it stops being pleasureful. The research supporting the model shows that, contrary to a tenacious myth, dopamine does not cause pleasure. Rather, dopamine is critical for the pursuit of goals, including the behaviors required to reach them and – most important– the powerful motivations needed to execute those behaviors. According to Berridge and colleagues, dopamine gets released from the midbrain in buckets when addicts are presented with cues associated with their substance of choice.

A sight, sound, or memory, reminiscent of that stuff (e.g., a cramp in the gut, the fleeting glimpse of someone who looks like a drug buddy, a scrap of paper dotted with a few flecks of white powder) will activate dopamine release and send it straight to the nucleus accumbens (NAcc; a major component of the ventral striatum) where it induces goal-oriented behavior (when the stuff is available) or craving (when it’s not).  But the power of cues to elicit the addictive impulse must take time to develop. It’s not present the first time you try drugs or booze, or even necessarily the 20th time. This process is therefore called incentive sensitization; because the cues that trigger drug seeking become sensitized over time.

The trouble is, Berridge and colleagues don’t explain how this sensitization takes hold. The cues must be processed somewhere in the back half of your brain (where “perception” first arises) and they must activate the amygdala, the famous limbic structure that produces emotional feelings on the basis of perception. But how do these perceptual and evaluative processes come to trigger the urge, the thrust, the powerful desire that is the essence of approach motivation? That would have to take place in the frontal cortex and its master motivator, the striatum.

Tomorrow we’ll look more closely at the phenomenon of kindling and how the two form a powerful neuroadaptive cycle within the brain.

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