On Mon, 2 Jun 2014 17:27:31 -0700 (PDT), Bruce Watson
Post by Bruce WatsonNicotine is not an MAO inhibitor. What does it do?
Nicotine, along with many other alkaloids and serotonin, is a tyramine
that is destroyed by monoamine oxidase. MAO inhibitors occurring in
tobacco, but not vaping juice, increase the bioavailability of
nicotine. That may explain why serum nicotine in smokers is 2-3 times
as high as vapers. I thought the explanation was size of aerosol
droplets (vaping droplets are much smaller), but it may be MAOIs.
Adding MAOIs to vaping juice would be an open invitation to FDA
regulation. It's not possible for political reasons.
I did not realize how similar nicotine is to serotonin were until
this thread prompted me to compare their molecular structures. Take a
look:
http://en.wikipedia.org/wiki/Serotonin
http://en.wikipedia.org/wiki/Nicotine
I used to think nicotine looked like acetylcholine. In fact, there is
no similarity.
http://en.wikipedia.org/wiki/Acetylcholine
Here is an answer to your question asking what nicotine does,
"Tobacco smoke contains the monoamine oxidase inhibitors harman,
norharman, anabasine, anatabine, and nornicotine. These compounds
significantly decrease MAO activity in smokers.MAO enzymes break down
monoaminergic neurotransmitters such as dopamine, norepinephrine, and
serotonin.
Nicotine also activates the sympathetic nervous system, acting via
splanchnic nerves to the adrenal medulla, stimulates the release of
epinephrine. cetylcholine released by preganglionic sympathetic fibers
of these nerves acts on nicotinic acetylcholine receptors, causing the
release of epinephrine (and norepinephrine) into the bloodstream.
By binding to ganglion type nicotinic receptors in the adrenal medulla
nicotine increases flow of adrenaline (epinephrine), a stimulating
hormone. By binding to the receptors, it causes cell depolarization
and an influx of calcium through voltage-gated calcium channels.
Calcium triggers the exocytosis of chromaffin granules and thus the
release of epinephrine (and norepinephrine) into the bloodstream. The
release of epinephrine (adrenaline) causes an increase in heart rate,
blood pressure and respiration, as well as higher blood glucose levels
Nicotine's mood-altering effects are different by report: in
particular it is both a stimulant and a relaxant.
First causing a release of glucose from the liver and epinephrine
(adrenaline) from the adrenal medulla, it causes stimulation.
When a cigarette is smoked, nicotine-rich blood passes from the lungs
to the brain within seven seconds and immediately stimulates the
release of many chemical messengers including acetylcholine,
norepinephrine, epinephrine, vasopressin, arginine, dopamine,
autocrine agents, and beta-endorphin.
This release of neurotransmitters and hormones is responsible for most
of nicotine's effects. Nicotine appears to enhance concentration and
memory due to the increase of acetylcholine. It also appears to
enhance alertness due to the increases of acetylcholine and
norepinephrine. Arousal is increased by the increase of
norepinephrine. Pain is reduced by the increases of acetylcholine and
beta-endorphin. Anxiety is reduced by the increase of beta-endorphin.
Nicotine also extends the duration of positive effects of dopamine and
increases sensitivity in brain reward systems.
At higher doses, nicotine enhances the effect of serotonin and opiate
activity, producing a calming, pain-killing effect. Nicotine is unique
in comparison to most drugs, as its profile changes from stimulant to
sedative/pain killer in increasing dosages and use."
http://www.bluelight.org/vb/threads/470385-Do-cigarettes-screw-with-your-serotonin-or-something