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

Copyright © 2011 Ivanhoe Broadcast News, Inc.