the science behind our addiction

Discussion created by MusicalHobbit on Aug 25, 2020
Latest reply on Aug 25, 2020 by Giulia

i found this a little earlier and thought i would share. this is fascinating. it talks about other drugs on this page too but i copied out the nicotine stuff.

not sure if it is due to my asperger's but i find a lot of scientific things very interesting and i love reading about stuff like how the brain works/is effected by things, and lots of other science stuff.

here we go.


Nicotine in Tobacco
Nicotine imitates the action of a natural neurotransmitter called acetylcholine and binds to a particular type of acetylcholine receptor, known as the nicotinic receptor.

Whether it is acetylcholine or nicotine that binds to this receptor, it responds in the same way: it changes its conformation, which causes its associated ion channel to open for a few milliseconds. This channel then allows sodium ions to enter the neuron, depolarizing the membrane and exciting the cell. Then the channel closes again, and the nicotinic receptor becomes temporarily unresponsive to any neurotransmitters. It is this state of desensitization that is artificially prolonged by continual exposure to nicotine.

Tobacco dependency, which then develops very quickly, arises because nicotinic receptors are present on the neurons of the ventral tegmental area which project their terminations into the nucleus accumbens. In smokers, repeated nicotine stimulation thus increases the amount of dopamine released in the nucleus accumbens. Between cigarettes, however, chronic smokers maintain a high enough concentration of nicotine to deactivate the receptors and slow down their recovery. This is why smokers develop a tolerance to nicotine and experience reduced pleasure from it.

After a brief period without smoking (a night’s sleep, for example), the baseline concentration of nicotine drops again, and some of the receptors regain their sensitivity. When all these receptors become functional again, cholinergic neurotransmission is raised to an abnormally high level that affects all the cholinergic pathways in the brain. Smokers then experience the agitation and discomfort that leads them to smoke another cigarette.

Another substance in tobacco smoke, not yet clearly identified, inhibits monoamine oxydase B (MAO B), an enzyme that breaks down dopamine after its reuptake. The result is a higher concentration of dopamine in the reward circuit, which also contributes to the smoker’s dependency.