Pharmacology - Nicotine - Useful pharmacology

[Jasim]

Neuropharmacology:

Nictone affects nicotinic acetylcholine receptors. Acetylcholine is a neurotransmitter involved in memory, muscular movement, and autonomic functioning in both the sympathetic and parasympathetic nervous systems. Acetylcholine also affects muscarinic receptors, the receptors affected by muscaria mushrooms. Nicotine does not affect muscarinic receptors, and muscaria does not affect nicotinic receptors.


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Effects on Metabolism and Drug Interactions:

Nicotine delays gastric empyting.
Anything in the stomach stays in the stomach longer. Since most drugs are absorbed more readily in the intestine, smoking may delay the onset of a drug. Some drugs (acidic drugs, such as aspirin) are absorbed more readily in the stomach. For such drugs nicotine may allow the drug to sit in the stomach longer, therefore increasing absorption.

Nicotine induces certain metabolic enzymes.
The cytochrome (cyp) P450 family of enzymes are involved in metabolizing a variety of drugs during Phase I metabolism. Metabolism of a drug generally deactivates that drug. When these enzymes are induced (or increased) there are more enzymes available to inactivate drugs. Nicotine induces specific cyp P450 enzymes, some of the key enzymes in drug metabolism. For drugs that are deactivated by these enzymes, nicotine use will decrease the duration of action. Certain drugs (called pro-drugs) must undergo metabolism in order to become active. For a pro-drug, nicotine use may help speed up the activation of the drug.


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Interesting Information:
In low doses nicotine can be a stimulant. In higher doses nicotine has more sedative properties.

It has been shown (need a source) that nicotine can improve memory. Swim has use nicotine (gum and cigs) before studying with good results.

Nicotine is speculated to help prevent alzheimer's disease.

Aspirin has a high affinity for depot binding sites. Swim has conducted the following experiment with great success: Take aspirin on an empty stomach. Smoke a cigarette to allow the aspirin to stay in the stomach and be absorbed (remember aspirin is an acidic drug and absorbs better in the stomach). Wait approximately 1 hour to 1 hour 20 mins. Take drug of choice with a full glass of room temp water (this will help to flush the drug to the small intestines. By this time the nicotine should not be affecting gastric emptying and the aspirin has bound to many depot binding sites, which usually sequester drugs and prevent them from acting. Swiy should notice an increased effect. Remember this works best on an empty stomach.


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Chemical Structures:

Nicotine: http://upload.wikimedia.org/wikipedi...D-skeletal.png

Acetylcholine: http://upload.wikimedia.org/wikipedi...s/4/40/ACh.png


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I hope some of this information will be useful. If anyone has anything to add, please share.
Nicotine is readily available and can be a way to modulate drug effects, but can also decrease a high if used without the knowledge of its effects on the body.

Reputation Comments on this post:

Thank you for this information on nicotine pharmacology. I always consider it to be beneficial to this forum as a compre...

[tryptamaster]

swim finds nicotine of basically no recreational value....he wonders y people ever started smokign dis shit in the first place. clearly cannabis was not native to europe or the americas or they wudnt have wasted thier lung cells on it

[Jasim]

My appologies if swim offended Switryptamaster. Swim's intent with this post was to simply share some information, not to advocate smoking. Swim thinks its a shame that due to the many negative effects of smoking, many benefits of nicotine are not well known.

[tryptamaster]

lol dont wry swiyasim. u didnt offend him. swim sjut doesnt know y people use nicotine.

[RaverHippie]

I was always interested in nicotine's neuropharmacology, nice post!

[Ilsa]

sweet post swijasim...there are in fact (and as you said) two broad classes of receptors (swim is drawing on distant memories of anatomy/neurobio in undergrad here so pardon any errors) that bind nicotine, dubbed nicotinic and muscarinic. the former are g-protein coupled receptors (GPCR's) that are coupled to more complex signalling pathways, whereas the latter are simple ion channels capable of eliciting an action potential (nerve impulse) all by themselves when stimulated by nicotine or other (hopefully more fun ) compounds.the GPCR's are more complex being that they rely on second messengers, but conversely they can be potentiated in ways the nicotinic receptors can't by amplification of the second messenger signal. very cool.

here's an informative link--esp as it relates to substances, including nicotine:

keep in mind though, through the exerimental evidence sections that these studies were a) done in rats and b) probably funded by some organization like NIDA and results will be skewed accordingly.

http://biopsychiatry.com/muscnic.htm

more later--swim is in need of a bong hit and a shower (just woke up--ya know your'e on df too much when posting comes before those two!!!

[Jasim]

Wow, thanks for the paper swiIlsa! Much of swim's work was done in the VTA of various strains of rats. Swim will try to find a copy of the complete paper, if anyone finds one, please share with swim

To clarify what swiIlsa was saying concerning the types of receptors. Nicotine affects the ionotropic nicotinic receptor. While muscarine affects the metabotropic muscarinic receptors. Swim remembers which is which from the alliteration of 'M'etabotropic 'M'uscarinic.

Ionotropic receptors are ion channels that go through the cellular wall. These channels open and close in response to their given chemical ligand (in this case nicotine). When the channels are open, ions quickly flow into the cell depolarizing the cellular membrane and causing a nerve impulse to fire. This is also called an 'action potential'.

Metabotropic receptors are much more subtle and take much longer to cause a biochemical reaction (a few seconds versus a few milliseconds for ionotropic). Again these receptors go through the cell membrane, but unlike the ionotropic receptors they do not have channels. Nothing can pass through a metabotropic receptor. When a chemical ligand binds to the outside portion of a metabotropic receptor, the inside portion changes shape, causing a biochemical cascade of events. This cascade of events can cause any number of changes to occur in the cell. Examples may include changing the amount of neurotransmitter being produced or release, causing channels to open and close in the cellular membrane, creating more receptors to put in the cellular membrane or removing receptors from the cellular membrane.


EDIT:
The fact that nicotinic receptors are ionotropic explains why nicotine is a stimulant in low doses, but a depressant in high doses. Swim will explain over the course of a cigarette: Nicotine binds to the ionotropic receptor and causes the nerve cells to fire. More and more nicotine comes in and causes more and more nerve cells to fire. This is the stimulant part. The nerve cells eventually become 'tired' and the ionotropic channels will no longer open in response to all the nicotine, nor will they open in response to the naturally occuring acetylcholine in the brain. This is the depressant part.

Reputation Comments on this post:

	nice clarification
	great information