Addiction - Dopamine - The Salience Theory

John (Gold)
John (Gold)

9:23 PM - Feb 03, 2005 #1

Addiction: Pay Attention
Psychology Today - Last Revised January 27, 2005

By: []Kathleen McGowan[/url]
Summary: Heroin and chocolate cake have a nasty way of crowding out the rest of the universe. The country's chief addiction expert argues that the propensity to drink, overeat and take drugs is a matter of attention gone awry.

Meeting her now, it is hard to believe that the Mexican-Russian great-granddaughter of the revolutionary Leon Trotsky ever felt the need to impress her friends. But the universal teenage urge to look more glamorous drove a young Nora Volkow, then in high school, to smoke her first cigarette. It could have been the first step toward a nasty habit, but something in her neurochemistry rebelled. She hated it.

Listening to her explain her theories about addiction and the brain, her self-diagnosis sounds right on target. Even though she's petite, with a jogger's lean physique, she dominates the room. She speaks very fast, with a Spanish accent that rounds her vowels, and ideas tumble out one after the other so quickly that it's almost impossible to keep up.

She's a fast-moving example of one of her most interesting theories: that addiction may be a malfunction of the normal human craving for stimulation. Volkow thinks that drugs and other addictive habits tap into some of the deepest forces within us--our lust for newness, our yearning for vitality and the deep-down thrill of being alive. "We all seek that intensity," she says. "There's something very powerful about that."

This idea is based on a new understanding of dopamine, the brain chemical involved in motivation, pleasure and learning. Because addictive drugs like cocaine and nicotine cause a flood of dopamine in the brain, researchers once thought that the neurochemical was a simple pleasure switch, the body's own "reward" button. Yet something didn't add up. If dopamine delivers the pleasure message, addicts should be in a continual state of bliss--but most of them get very little pleasure from the drug, despite the surge of neurochemicals. "I've seen hundreds of addicted people, and never have I come across one who wanted to be addicted," says Volkow. As she began doing brain-imaging studies with drug addicts, that contradiction haunted her.

In response, Volkow and other researchers are developing a new understanding of addiction. Rather than just telling us to feel good, dopamine tells us what's salient--the unexpected bits of new information we need to pay attention to in order to survive, like alerts about sex, food and pleasure, as well as danger and pain. If you are hungry and you get a whiff of a bacon cheeseburger, Volkow's research team has shown, your dopamine skyrockets. But the chemical will also surge if a lion leaps into your cubicle. Dopamine's role is to shout: "Hey! Pay attention to this!" Only as an afterthought might it whisper "Wow, this feels great." So maybe addicts aren't just chasing a good time. Perhaps their brains have somehow mistakenly learned that drugs are the most important thing to pay attention to, as crucial to survival as food or sex.

The salience theory of dopamine also provides new explanations for other self-destructive human tendencies, from binge eating to gambling. It may explain why we crave the stimulation of new information. The experiments that Volkow and her team are conducting may also reveal some of the most powerful behavioral machinery in our brains, the equipment that motivates and inspires us. If they are right, dopamine is more than a joyride. It's more like the drug of life. Its mission is more profound and philosophical: to connect us to the world and supply us with the will to stay alive.

Nora Volkow, now 48, has science in her blood. Her father is a chemist, her grandfather and her great-grandfather were physicists. But her family, which emigrated from Russia to Mexico in the 1930s, has another intellectual legacy. One of her great-grandfathers was the brilliant Bolshevik leader Leon Trotsky, and Volkow grew up in the Mexico City home where he spent the last days of his life--and where he was killed on Stalin's orders in 1940. Parts of the house became a museum of Trotsky's life, and when Volkow was a child, people like the Nobel Prize-winning novelist Gabriel Garcia Marquez would stop by.

Volkow, though, was more interested in psychiatry than in politics. She graduated at the top of her medical school class at the National University of Mexico, then came to the United States to pursue the new science of brain imaging. During the 1980s, at New York University and then at University of Texas, Austin, she used brain imaging techniques to study schizophrenia and cocaine addiction--and established herself as a leader in the field. She then moved to Brookhaven National Laboratory in Upton, New York, where she won a reputation as an intellectual powerhouse, respected for her creativity as well as for her productivity. "Nora has that enthusiasm, that spark," says NYU Medical Center psychiatry chair Robert Cancro, who worked with her early in her career. "She'd get excited about things, talk 160 words a minute--and that was in English!"

Her colleagues say she is a bold and unconventional thinker. Early on, she demonstrated that cocaine physically damaged the brain. It took years before this controversial finding was accepted, but other research eventually proved her right. She was also an early champion of the idea that drug addiction is a medical problem, rather than a lack of willpower or moral fiber. That formerly radical view is now considered mainstream.

Since she was chosen to direct NIDA last year, Volkow has brought new visibility to the controversial theory about dopamine that has percolated in the scientific community for approximately the past decade. According to the salience theory of dopamine, the neurochemical is released when something surprisingly important happens, whether that's an unexpected reward or accidentally stepping on a nail. Since dopamine is also involved in learning, memory and motivation, the chemical helps us pay attention to the information we need to survive, act upon it, and remember it for the future. But drugs hijack that machinery, sending 5 to ten times as much dopamine surging through the nucleus accumbens and forcing the brain's motivational and attentional mechanisms to focus purely on the drug. It becomes the most interesting and important thing in the world. "In any addicted person, what's salient is the drug," says Volkow. "There's no competition."

Over time, the addict's brain adapts to the torrent of dopamine by dampening the system down. Imaging experiments show that cocaine addicts' brains don't react to the things that turn on the rest of us, whether that's romantic passion, food or cold, hard cash. Volkow's research has also shown that addicts have fewer dopamine D2 receptors, which are found in parts of the brain involved in motivation and reward behavior. With fewer receptors, the dopamine system is desensitized, and the now-understimulated addict needs more and more of the drug to feel anything at all. Meanwhile, pathways associated with other interesting stimuli are left idle and lose strength. The prefrontal cortex--the part of the brain associated with judgment and inhibitory control--also stops functioning normally. It's a neurological recipe for disaster. "You have enhanced motivation for the drug, and you have impaired prefrontal cortical systems. So you want the drugs pathologically, and you have reduced control of behavior, and what you've got is an addict," says University of Michigan, Ann Arbor psychology professor Terry Robinson, who pioneered this new way of thinking about dopamine with his University of Michigan colleague Kent Berridge.

Some people are apparently born with fewer dopamine receptors, and they are more likely to enjoy the rush of addictive drugs. In one imaging experiment, Volkow gave Ritalin, which gently lifts dopamine levels, to a group of ordinary volunteers. Some loved the feeling of the drug, but others hated it so much that they threatened to drop out of the study. Volkow was puzzled until she imaged their brains. She found that those who liked the rush from the drug had fewer dopamine D2 receptors than those who hated it. Volkow thinks that some people have a sensitive dopamine circuitry; they can't take the additional stimulation of drugs.
Obesity may involve similar malfunctions in the dopamine system. Volkow's longtime Brookhaven collaborator Gene-Jack Wang has discovered that the brains of seriously obese people seem to be tuned toward food. Even when they are lying quietly in the scanning machine, the sensory cortex of their mouth, tongue and lips is more active than it is in normal-weight people, he says: "They are putting out their antennae." Yet he also found that the dopamine circuitry of heavy people is less responsive, with fewer dopamine D2 receptors. Even among the obese, there are dopamine differences. The heaviest people in his study had fewer dopamine receptors than the lightest. Like addicts, overeaters may be compensating for a sluggish dopamine system by turning to the one thing that gets their neurons pumping.

It's a mark of changing times--and more sophisticated science--that the head of the National Institute on Drug Abuse is thinking about doughnuts as well as heroin. Just as blaming drug addiction on moral weakness was a shortsighted and unscientific way of framing a social problem, Volkow believes that focusing solely on metabolism, or blaming fat people for overindulgence and gluttony, are intellectual dead ends. "What motivates us to eat is clearly much more than hunger," she says. "We need to expand the way we think about eating." Wang and Volkow suggest that dopamine may provide a new window into weight loss: Animal studies have shown, for example, that exercise elevates dopamine release and increases dopamine D2 receptors.

Volkow and the other champions of the new view of dopamine don't deny that the chemical helps us register pleasure. But they think that pleasure is just part of a set of interconnected dopamine-related behaviors. Volkow recently found that adults with attention deficit disorder who took dopamine-boosting Ritalin before taking a math test found it easier to concentrate, in part, because the task seemed more interesting, so they felt more motivated to do the problem.

From this angle, it makes sense that the cognitive process of absorbing new information is closely tied to the brain's pleasure mechanisms. You might say that what the brain really "wants" is new information, suggests Gregory Berns, associate professor of psychiatry and behavioral sciences at Emory University in Atlanta. "Neurons really exist to process information. That's what neurons do. If you want to anthropomorphize neurons, you can say that they are happiest when they are processing information."

This urge to connect to the world and learn from it is more important than mere pleasure, says Volkow. It's part of the most basic force in behavior: the will to live. It's not automatic, she points out. Seriously ill or very depressed people can lose the will to survive. "What is the motivation we all have to be alive, to do things?" she asks. "It's not pleasure. Our lives would be so much simpler if we were motivated just for the sake of pleasure."

But dopamine sensitivity and addiction aren't genetically determined or inevitable. One experiment with monkeys showed that the dopamine system may be influenced by social interactions: Animals that lost social status also lost D2 receptors. Context is also crucial. Obviously, it's easier to get hooked if drugs are easy to get in your neighborhood, but it's not just a question of supply and demand. People who grow up in stimulating, engaging surroundings are protected against addiction, Volkow believes, even if they don't have a naturally responsive dopamine system. If you connect to the world in a meaningful way, and have more chances to get excited about natural stimuli, you're less likely to need an artificial boost.

"If you don't get excited by everyday things in life, if things look gray, and the drug makes things look extraordinary, that puts you at risk," she says. "But if you get great excitement out of a great multiplicity of things, and intensely enjoy these things--seeing a movie, or climbing a mountain--and then you try a drug, you'll think: What's the big deal?" For those lucky enough to grow up as Volkow did, surrounded by sharp minds and fascinating history, drugs are just nowhere near as interesting as everyday life.

Source Link:
Psychology Today Magazine © Copyright 1991-2005
Note: All images added by John R. Polito
Last edited by John (Gold) on 2:39 AM - Feb 17, 2009, edited 2 times in total.


9:54 PM - Feb 03, 2005 #2

John, this is certainly powerful information. As an addict, it rings very true. No one who is addicted really enjoys the addiction. This scientific information certainly sheds new light on the panic an addict feels at the thought of giving up the drug. As a newbie, I am already astonished to think about how much I thought I NEEDED nicotine and how it feels like a distant memry that I can only vaguely recall now; only a month quit! The calmness and peace come as such an unexpected surprise.
Thank you again for all you do here. Addiction is addiction is addiction and it can kill. I feel so alive and well and grateful today. NTAP
Free and Healing for One Month, Two Days, 9 Hours and 23 Minutes, while extending my life expectancy 2 Days and 19 Hours, by avoiding the use of 810 nicotine delivery devices that would have cost me $121.63.


12:36 AM - Feb 04, 2005 #3

Thank you John. This is food for thought and apparently thinking will help to keep me from smoking. If accurate, this explains a lot of things to me.


IrishLotus GOLD
IrishLotus GOLD

1:05 AM - Feb 04, 2005 #4

Thanks for this intriguing article John. It seems I have been endlessly interested in this link between dopamine and my addictive behaviors. Especially since I think I have finally started to get those "natural" dopamine surges back under my control. Of course, that's a good thing! After all, it seems I am currently experiencing the rush of dopamine associated with learning new things. Who woulda thunk it! It certainly feels better than any rush I ever got from sucking off a sickarette. Thanks again John! You're the best!
YQS~Mary Kate
Free and very gratefully healing 2 Years, 4 Months, 11 Days, 7 Hours and 38 Minutes, while extending my life expectancy 89 Days and 22 Hours, by avoiding the use of 25900 nicotine delivery devices that would have cost me $6,710.14. And learning something new about myself every day!
Last edited by IrishLotus GOLD on 2:41 AM - Feb 17, 2009, edited 1 time in total.


1:52 AM - Apr 28, 2006 #5

This is very interesting information and kinda like throws light on those times I have been so knee deep into learning something new that I haven't once thought or required a cigarette! And how when very bored I would smoke and smoke....
Also throws light on how when quitting many recommend getting busy, learning a new skill

John (Gold)
John (Gold)

8:13 PM - May 16, 2006 #6

Addiction's grip now seen as 'extreme memory'
The Boston Globe
By Carey Goldberg, Globe Staff | May 15, 2006
Explain this: An addict sweats through withdrawal. He commits to staying sober. With years of effort, he builds a life he loves. And then, one day, he passes his old shooting alley or gets pain pills from the dentist, and boom. Relapse. It all comes crashing down. By all accounts, something similar may have hit US Representative Patrick Kennedy earlier this month.

Old theories of addiction seem to fall short here. If the essence of addiction is dependence on a drug and fear of withdrawal symptoms, then why should this happen to a man who long since went through withdrawal? Or if addiction is about pleasure, why should a man embark on a course that will surely bring nothing but pain?

Last week, brain scientists gathered at the Massachusetts Institute of Technology batted around a newer theory that could fit a few more pieces into the puzzle and is already spurring experiments on new potential treatments.

The idea is that addiction may be a form of ''extreme memory" or ''pathological learning." And that addiction can be so potent and persistent because it takes over learning processes in the brain that are central to humans' very survival.

The brain evolved to identify essentials such as food or water and to record exactly how they can be reached, said Dr. Steven E. Hyman, a neuroscientist who is provost of Harvard University. And when it finds -- or even only expects to find -- such essentials, the chemical messenger dopamine is released. Its job in the brain is to say: ''This is very important; let's remember exactly how we did this."

Even though they provide no benefit to the body, drugs can usurp that system, he said, by releasing dopamine -- so much dopamine, in fact, that little else can compete, leading addicts' brains to ''overlearn" the false message that drugs are good.

Those surges of dopamine, the theory goes, contribute to the laying down of long-term memories and associations that remodel the connections in the brain and can last forever.

Last year Hyman published a review article called ''Addiction: A Disease of Learning and Memory" in the American Journal of Psychiatry and concluded that neuroscience was reaching ''a far more accurate and robust picture of addiction than we had a few short years ago."

Scientists who spoke at the MIT forum, held at the Picower Institute for Learning and Memory, cautioned that addiction is hideously complex and the memory aspect is surely only a piece of it.

But the ''extreme memory" idea has been gaining attention among researchers in the last several years, they said, raising hopes that they may be able to apply some of the recent scientific progress on understanding memory at a molecular level to the conundrum of addiction

Already, researchers working with animals are trying out drugs that affect memory to see whether they can help treat addiction, said Dr. Nora Volkow, director of the federal National Institute on Drug Abuse

The institute is funding several studies that treat ''addicted" rodents with drugs that allow the replacement of old memories with new and different ones. The idea, Volkow said, is to break the power of cues that can cause relapse.

For example, she said, a rat can be conditioned to associate a certain place with cocaine. But if it is given a drug that ''breaks" old memories as they come up again, a new no-cocaine memory may replace the cocaine one, breaking the association in the animal's brain between the place and the drug.

Researchers hope that such memory-altering medications might even ''erase the memory of the pleasure associated with the drug," she said.

One medication that has shown promise in breaking associations, even in humans, is D-Cycloserine, which is commonly used at higher doses for tuberculosis. Experiments have shown that it might be an effective treatment for phobias. At this point, however, the studies are too new to tell whether memory drugs will work for addictions, Volkow said.

Recent research on the genes associated with addiction also seems to support the theory that learning and memory play an important role, Volkow said.

In animals, when researchers manipulate genes involved in long-term learning, they create changes in the animals' response to drugs of abuse, she said, ''suggesting to investigators that these genes may be important in regulating the vulnerability to addiction."

Other animal studies have shown that addictive drugs have dramatic effects on learning circuits, researchers said.

A key to understanding addiction is to understand why and where such changes occur in learning circuits, said Dr. Robert C. Malenka, a neuroscientist at Stanford University. ''And if we understand that, maybe we'll be able to develop therapies that could begin to reverse them."

As this ''pathological learning" model gains force, it may help reduce some of the stigma of addiction, some at the Picower conference said. Addiction, according to this model, is nothing so simple as a weakness of will, they said.

The new model also provides a possible biological underpinning for aspects of the disease that addicts and those who treat them have long observed, said Dr. Shelly F. Greenfield, associate clinical director of the Alcohol and Drug Abuse Treatment Program at McLean Hospital.

''We often think of treatment as quitting and staying quit," she said. ''Most people, I think, would agree that the quitting part is easier than the staying quit."

Carey Goldberg can be reached at [][/url].
© Copyright 2006 Globe Newspaper Company
Online Source Link:
Thanks to Joseph for bringing this article to our attention!

John (Gold)
John (Gold)

10:54 AM - Mar 09, 2007 #7

Pay Attention Cycle
Last edited by John (Gold) on 2:35 AM - Feb 17, 2009, edited 1 time in total.

John (Gold)
John (Gold)

12:30 AM - Mar 19, 2007 #8

Time to Quit Smoking? by []John R. Polito[/url]

Want to quit smoking but feeling unable? Drug addiction is about the brain's "pay attention" dopamine pathways being taken hostage by an external chemical. These pathways were engineered to teach and reinforce species survival priorities associated with food, water, nurturing, accomplishment and reproduction. Enter nicotine, the most perfectly designed drug of addiction.

Nicotine not only fosters dopamine flow but turns off a key killjoy enzyme that prevents its cleanup. It results in a powerful "aaah" sensation within seconds of a puff that lingers far longer than normal. The entire event gets recorded in what may be the highest definition memory the mind can produce. Continued smoking by the new smoker causes these extremely salient memories to quickly pile up. They soon bury all remaining memory of life without it. The now dependent user becomes totally yet falsely convinced that life without nicotine isn't nearly as good, that it defines who they are, that it provides their edge in life.
As if that isn't enough, the brain's physiology fights back by growing millions of extra nicotinic-type acetylcholine receptors in at least eleven different brain regions, almost as if trying to more widely disburse arrival of the super-toxin nicotine. It's called "tolerance" and causes the new nicotine addict to need to smoke a bit more to achieve the previously remembered effect. Two cigarettes a day, five, ten, the brain grows additional receptors requiring the smoker to puff more, deeper, harder or hold it longer.

Now any attempt to stop using nicotine is met with a rising tide of powerful anxieties inside a mind left briefly de-sensitized to its own natural neurochemical flow. Rewired to function with nicotine present, the brain now needs time to reverse the process and down-regulate receptor counts.

As if that isn't enough, a never-ending cycle of nicotine replenishment causes the smoker to establish recorded nicotine replenishment patterns associated with smoking during various activities, at specific locations, at certain times, in the presence of particular people or when experiencing various emotions. This classical conditioning, like Pavlov's dogs salivating upon hearing a bell ring, must now be extinguished for each established cue. Encountering each trigger may generate a brief yet powerful anxiety episode lasting less than three minutes. But recovery time distortion can make the minutes feel like hours.

Nicotine addiction is about living a lie. It's about forgetting the amazingly calm and quiet mind we once called home. It's about "pay attention" pathways responding to dopamine overload by creating a new #1 priority in life - obtaining that next fix. The smoker may forget to take their vitamin or medicine, procrastinate regarding work, skip meals, family time, or even romance but they will not forget or skip that next mandatory feeding.

Key to enhancing your ability to return home is knowledge, some form of ongoing support and an appreciation that just one powerful puff of nicotine and relapse is all but assured. Like an alcoholic trying to toy with "just one sip," treating a true chemical addiction as though it were some "nasty little habit" is a recipe for relapse. We call it the "Law of Addiction" and if broken, all your hard work and dreams will again find themselves back behind bars.

Take your own poll of former smokers. Contrary to the assertions of those selling quitting aids, about 90% of all long-term successful ex-smokers quit smoking cold turkey. It's fast, clean, free and it works. But abrupt nicotine cessation doesn't mean quitting in ignorance and darkness. The Internet is loaded with free quality resources. When ready, simply type "quit smoking cold turkey" into your favorite search engine.

Remember, knowledge truly is power. Trying to quit in darkness when you can turn on the lights is like trying to land a plane without putting the wheels down. It can be done but why even try? In the end there's just one principle that if followed provides a 100% guarantee of success to all ... no nicotine just one day at a time, Never Take Another Puff, Dip or Chew!

About the author: []John R. Polito[/url], a former 30-year three pack-a-day smoker, is editor of, the Internet's oldest forum devoted exclusively to teaching the art, science and psychology of abrupt nicotine cessation. The site is staffed entirely by volunteer counselors, is totally free and declines all offers of donations.

Related Reading
  • WhyQuit - The Internet's oldest forum devoted to the art, science and psychology of abrupt nicotine cessation
  • Joel's Reinforcement Articles - 95 short stop smoking articles on every recovery topic imaginable
  • "Never Take Another Puff" - a PDF book containing all 95 Reinforcement articles
  • Freedom from Tobacco - an online peer education and support forum
  • Joel's Video and Audio Quit Smoking Lessons - Movie and sound clips in which Joel shares a host of important nicotine dependency recovery lessons
  • Daily Quitting Lesson Guide - This guide suggests daily video and reading lessons for specific days during the first two weeks
  • Ask Joel - A forum where you can ask America's leading nicotine cessation counselor your quitting question
  • 50 Quitting Tips - A short summary of quit smoking tips
Link to 03/18/07 release of Time to quit smoking?
Last edited by John (Gold) on 2:48 AM - Feb 17, 2009, edited 1 time in total.

forza d animo
forza d animo

12:58 AM - Oct 06, 2007 #9

While this is a very lengthy article and may take several reads to absorb all that it offers, it is worth reading. There are several articles in this string that shed light on addiction. It is this type of information that is offered here that you will find at no other "smoking cessation site" We are about nicotine cessation. We smoked because we are drug addicts addicted to nicotine.

From Nora Volkow above:
"If you don't get excited by everyday things in life, if things look gray, and the drug makes things look extraordinary, that puts you at risk," she says. "But if you get great excitement out of a great multiplicity of things, and intensely enjoy these things--seeing a movie, or climbing a mountain--and then you try a drug, you'll think: What's the big deal?"

Recovery is life affirming. Enjoy it and you will heal more quickly!

Gold x2.98


4:06 AM - Oct 07, 2007 #10

This all makes so much sense to dopamine circuitry is all messed up! Started out with chronic clinical depression age 7. Started overeating, overweight until age 14 when I started smoking. Drank and drugged my way to 1st rehab age 21. Etc Etc Etc. Could be why I'm still mentally craving sickarettes at age 51, 1.5 months nicotine free? Grrrrrrrrr!!! Suzi 1M 15D


12:13 AM - Oct 31, 2007 #11

Hmmm....(rubs chin thoughtfully)

...perhaps that's why this group is so effective at keeping people quit: we become fascinated by the entire process of quitting, we get a greater and greater sense of acheivement as each day goes by and a greater appreciation of real life. Learning to live without nicotine is learning a new skill and one begins to truly see that

'..drugs are just nowhere near as interesting as everyday life.'

Sean - living in the light for Three months, one day, 8 hours, 43 minutes and 19 seconds. 2800 cigarettes not smoked, saving £144.78. Life saved: 1 week, 2 days, 17 hours, 20 minutes.

John (Gold)
John (Gold)

8:53 AM - Nov 06, 2007 #12

Exposure to nicotine and sensitization of nicotine-induced behaviors
Prog Neuropsychopharmacol Biol Psychiatry. 2007 September 1; [Epub ahead of print]

Vezina P, McGehee DS, Green WN.
Department of Psychiatry, The University of Chicago, 5841 S. Maryland Avenue, MC3077, Chicago, IL 60637, United States.

Evidence for an important link between sensitization of midbrain dopamine (DA) neuron reactivity and enhanced self-administration of amphetamine and cocaine has been reported. To the extent that exposure to nicotine also sensitizes nucleus accumbens DA reactivity, it is likely that it will also impact subsequent drug taking. It is thus necessary to gain an understanding of the long-term effects of exposure to nicotine on nicotinic acetylcholine receptors (nAChRs), neuronal excitability and behavior.

A review of the literature is presented in which different regimens of nicotine exposure are assessed for their effects on upregulation of nAChRs, induction of LTP in interconnected midbrain nuclei and development of long-lasting locomotor and DA sensitization. Exposure to nicotine upregulates nAChRs and nAChR currents and produces LTP of excitatory inputs to midbrain DA neurons. These effects appear in the hours to days following exposure. Exposure to nicotine also leads to long-lasting sensitization of nicotine's nucleus accumbens DA and locomotor activating effects. These effects appear days to weeks after drug exposure. A model is proposed in which nicotine exposure regimens that produce transient nAChR upregulation and LTP consequently produce long-lasting sensitization of midbrain DA neuron reactivity and nicotine-induced behaviors. These neuroadaptations are proposed to constitute critical components of the mechanisms underlying the initiation, maintenance and escalation of drug use.

Joined: 7:22 PM - Nov 11, 2008

3:04 PM - Mar 12, 2011 #13

The below 1998 dopamine pleasure versus wanting study abstract should be part of this thread as it is the earliest paper I've seen on the topic and provides the foundation science for much of the above.  The word "hedonic" as used the below study summary means "of, relating to, or marked by pleasure." 

Seventy percent of surveyed smokers state that they want to quit.  Does that sound like smoking is about like, love or pleasure?  But it's entirely normal when seeing ourselves do something over and over and over to think and feel that there must be some like, love or pleasure to it, or else why would we do it again?   This line of research suggests that the urges felt are about satisfying dopamine pathway want and desire, not love, like or pleasure, that the "aaah" sensation sensed within ten seconds of a puff is actually relief from neuro-chemically generated want.

Although a lot to swallow, what's simple is knowing that it is impossible to relapse so long as no nicotine enters this bloodstream!

Breathe deep, hug hard, live long,

John (Gold x11)

What is the role of dopamine in reward:
hedonic impact, reward learning,
or incentive salience?

Journal:  Brain Research. Brain Research Reviews, December 1998, Volume 28(3), Page 309-369.

Authors:  Berridge KC, Robinson TE.

Department of Psychology, University of Michigan, Ann Arbor, MI 48109-1109,

"What roles do mesolimbic and neostriatal dopamine systems play in reward? Do they mediate the hedonic impact of rewarding stimuli? Do they mediate hedonic reward learning and associative prediction? Our review of the literature, together with results of a new study of residual reward capacity after dopamine depletion, indicates the answer to both questions is 'no'. Rather, dopamine systems may mediate the incentive salience of rewards, modulating their motivational value in a manner separable from hedonia and reward learning.

In a study of the consequences of dopamine loss, rats were depleted of dopamine in the nucleus accumbens and neostriatum by up to 99% using 6-hydroxydopamine. In a series of experiments, we applied the 'taste reactivity' measure of affective reactions (gapes, etc.) to assess the capacity of dopamine-depleted rats for: 1) normal affect (hedonic and aversive reactions), 2) modulation of hedonic affect by associative learning (taste aversion conditioning), and 3) hedonic enhancement of affect by non-dopaminergic pharmacological manipulation of palatability (benzodiazepine administration).

We found normal hedonic reaction patterns to sucrose vs. quinine, normal learning of new hedonic stimulus values (a change in palatability based on predictive relations), and normal pharmacological hedonic enhancement of palatability. We discuss these results in the context of hypotheses and data concerning the role of dopamine in reward. We review neurochemical, electrophysiological, and other behavioral evidence.

We conclude that dopamine systems are not needed either to mediate the hedonic pleasure of reinforcers or to mediate predictive associations involved in hedonic reward learning. We conclude instead that dopamine may be more important to incentive salience attributions to the neural representations of reward-related stimuli. Incentive salience, we suggest, is a distinct component of motivation and reward. In other words, dopamine systems are necessary for 'wanting' incentives, but not for 'liking' them or for learning new 'likes' and 'dislikes'."

PubMed Link:

Below is a more recent paper by Berridge

The debate over dopamine's role in reward:
the case for incentive salience.
Psychopharmacology (Berlin). 2007 Apr;191(3):391-431. Epub 2006 Oct 27.

Berridge KC.

Department of Psychology, University of Michigan, 530 Church Street (East Hall), Ann Arbor, MI 48109, USA. [][/url]

Abstract INTRODUCTION: Debate continues over the precise causal contribution made by mesolimbic dopamine systems to reward. There are three competing explanatory categories: 'liking', learning, and 'wanting'. Does dopamine mostly mediate the hedonic impact of reward ('liking')? Does it instead mediate learned predictions of future reward, prediction error teaching signals and stamp in associative links (learning)? Or does dopamine motivate the pursuit of rewards by attributing incentive salience to reward-related stimuli ('wanting')? Each hypothesis is evaluated here, and it is suggested that the incentive salience or 'wanting' hypothesis of dopamine function may be consistent with more evidence than either learning or 'liking'.

In brief, recent evidence indicates that dopamine is neither necessary nor sufficient to mediate changes in hedonic 'liking' for sensory pleasures. Other recent evidence indicates that dopamine is not needed for new learning, and not sufficient to directly mediate learning by causing teaching or prediction signals. By contrast, growing evidence indicates that dopamine does contribute causally to incentive salience. Dopamine appears necessary for normal 'wanting', and dopamine activation can be sufficient to enhance cue-triggered incentive salience. Drugs of abuse that promote dopamine signals short circuit and sensitize dynamic mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Such drugs interact with incentive salience integrations of Pavlovian associative information with physiological state signals. That interaction sets the stage to cause compulsive 'wanting' in addiction, but also provides opportunities for experiments to disentangle 'wanting', 'liking', and learning hypotheses. Results from studies that exploited those opportunities are described here.

CONCLUSION: In short, dopamine's contribution appears to be chiefly to cause 'wanting' for hedonic rewards, more than 'liking' or learning for those rewards.

PMID: 17072591 [PubMed - indexed for MEDLINE]

PubMed Link:
Last edited by JohnPolito on 3:11 PM - Mar 12, 2011, edited 1 time in total.

Joined: 7:22 PM - Nov 11, 2008

1:45 PM - May 05, 2011 #14

Reported May 5, 2011 Nicotine and Cocaine: Similar Addiction? Medical Breakthroughs - Reported by Ivanhoe

(Ivanhoe Newswire) -- New research from the University of Chicago Medical Center has given new insight into just what makes cocaine and nicotine so addictive. According to the research, the effects of nicotine on the regions of the brain associated with addiction are similar to those of cocaine—both create lasting changes in a person’s brain by affecting similar mechanisms of memory on first contact.

Scientists have already established that learning and memory are connected to one another via “synaptic plasticity”—the long-term strengthening and weakening of connections between neurons. The more often two neurons are activated together, the stronger the bond between them becomes. This leads to an increased ability for one neuron to excite the other.

Previous research by Daniel McGehee, Ph.D., at the University of Chicago Medical Center has also shown that nicotine can promote plasticity in the region of the brain called the ventral tegmental area, or VTA. Neurons originating from the VTA release dopamine, a neurotransmitter that plays a role in rewards, such as food and sex, and addictions. In a series of new experiments, Danyan Mao, Ph.D., also of the University of Chicago Medical Center, monitored the electrical activity of VTA dopamine neurons in slices of brain taken from adult rats. Every slice was soaked for 15 minutes in a concentration of nicotine that equaled the amount that would reach the brain after smoking one cigarette. After 3 to 5 hours, experiments were conducted in order to detect the presence of synaptic plasticity and find out which neurotransmitter receptors were involved in the development of the synaptic plasticity.

As a result of the experiment, Mao discovered two receptors necessary for synaptic plasticity in the VTA: the acetylcholine receptor located on the dopamine neurons, and the D5 dopamine receptor—a component previously associated with the consumption of cocaine. If either of these receptors were blocked during nicotine exposure, the drug’s ability to cause lasting changes in excitability was eliminated.

The findings from the experiment suggest a reason for why both cocaine and nicotine are such highly addictive substances. Daniel McGehee, Ph.D., neuroscientist and associate professor in the Department of Anesthesia & Critical Care at the Medical Center, was quoted as saying,

“We know without question that there are big differences in the way these drugs affect people. But the idea that nicotine is working on the same circuitry as cocaine does point to why so many people have a hard time quitting tobacco, and why so many who experiment with the drug end up becoming addicted.”

While the results of the experiment also pose possible strategies for preventing or treating cocaine and nicotine addictions, the use of D5 blockers to treat addiction may be further in the future—currently all known blockers of the D5 receptor also block the D1 dopamine receptor, which is important for healthy motivation and movement.

Ivanhoe Story Source: Journal of Neuroscience, May 4, 2011
Online link: ... ryid=26959

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