First off, be sure to understand that there is a huge difference between nicotine alone and smoking tobacco. There are over 1000 chemicals produced when smoking tobacco so theoretically any or all of these could have psychoactive effects. The main thing to keep in mind is that smoked tobacco contains MAOIs.
http://en.wikipedia.org/wiki/MAOIs
Second, nicotine is a nAChR agonist. Nicotine binds to acetylcholine receptors (of the nicotinic type) because it is shaped somewhat like acetylcholine. However because it is not acetylcholine its shape allows it only to bind to the nAChR receptor type (as opposed to the other type of acetylcholine receptor mAChR; of which acetylcholine also binds but nicotine can not). These receptors are located on a variety of neurons that release various things including hormones, neurotransmitters, and others.
There are some neurons that when acetylcholine binds to, release dopamine. It should be noted that just some of the neurons that nicotine binds to release dopamine. I'm not sure, but I believe more adrenaline and noradrenaline are released compared to dopamine.
Third, dopamine is "inactivated" by enzymes called MAO. MAOIs in smoke inhibit these MAOs causing more dopamine, noradrenaline, adrenaline, serotonin, and other neurotransmitters/hormones to activate receptors.
Fourth, any excess receptor activation usually causes downregulation. So regardless of nicotine-only substances or smoking, receptors will downregulate; though smoking will downregulate them faster.
Finally, nicotinic receptors are sensitive, moreso than most all other receptors. Essentially, nicotine hits them "harder" then the natural acetylcholine and after a certain amount of getting hit hard, they die (sometimes called inactivated). If one starts a cigarette they feel stimulated. That's the beginning of unnatural release of neurotransmitters (well conditioning is also involved in this release, but I'll leave that out). Slowly the user gains more of a release of receptor activation (usually reported as euphoria).
As you have been taught, this is oversimplified to dopamine activation. However like I stated before, there are nicotinic receptors on all types of neurons so the answer is not nearly that simple.
So the user gets towards the end of a cigarette. At this point a lot of nAChRs have been deactivated (killed). However the combination of MAOIs keep receptor activation going for dopamine, serotonin, noradrenaline, and epinephrine. So you still feel good. Slowly, the constant unnatural activation causes these receptors to downregulate. Particularly dopamine, noradrenaline, and epinephrine. So now there are less of these receptors to be activated. At the same time MAOI levels are diminishing leading to less levels of catecholamines (dopamine, noradrenaline, and adrenaline).
The combination of nicotinic receptor inactivation, receptor downregulation, and low levels of neurotransmitters is responsible for both the sedative effects of nicotine and part of the withdrawal symptoms. The difference between the sedative and withdrawal symptoms is only one of degree.
As you can see, the are many factors involved. One that I didn't mention was the fact that there are nAChRs on GABA receptors. These release more GABA. In relation to nicotine's effects on opioids, I've read that nicotine increases opioid concentrations in some parts of the brain while decreasing it in others. What is known is that nicotine sensitizes the reward system of the brain, fucks with your natural brain system, and has a high probability of causing cancer.
Regarding the amps, I've had the exact same thing happen. Just stay away form the cigarettes unless you plan on smoking at least a pack a day. I believe it to be rapid downregulation of catcholamine receptors from the combination of releasing from the amps and MAO inhibition from the MAOIs.
When you get down to it you're mixing poison with speed, what'd you expect?
