Drugs:Fact and Fiction/Nicotine
Any of various drugs that inhibit, enhance, or mimic the action of the neurotransmitter acetylcholine, the primary transmitter of nerve impulses within the parasympathetic nervous system—i.e., that part of the autonomic nervous system that contracts smooth muscles, dilates blood vessels, increases bodily secretions, and slows the heart rate. Some cholinergic drugs, such as muscarine, pilocarpine, and arecoline, mimic the activity of acetylcholine in stimulating the parasympathetic nervous system. These drugs have few therapeutic uses, though one of them, nicotine, is the principal addictive ingredient in the tobacco used in cigarettes and cigars. Other cholinergic drugs, such as atropine and scopolamine, inhibit the action of acetylcholine and thus suppress all the actions of the parasympathetic nervous system. They are used therapeutically to diminish salivation and bronchial secretions during anesthesia and to dilate the pupil during ophthalmological procedures. Scopolamine is also used to treat motion sickness, an effect that depends on its ability to depress the activity of the central nervous system.
Taken from Britannica.com's inquiry of Cholinergic Drugs
Cholinergic receptors are present in many brain structures, as well as in muscles, adrenal glands, the heart, and other body organs. These receptors are normally activated by the neurotransmitter acetylcholine, which is produced in the brain, and by neurons in the peripheral nervous system. Acetylcholine and its receptors are involved in many activities, including respiration, maintenance of heart rate, memory, alertness, and muscle movement.Because the chemical structure of nicotine is similar to that of acetylcholine's, it is also able to activate cholinergic receptors. But unlike acetylcholine, when nicotine enters the brain and activates cholinergic receptors, it can disrupt the normal functioning of the brain.
Regular nicotine use causes changes in both the number of cholinergic receptors and the sensitivity of these receptors to nicotine and acetylcholine. Some of these changes may be responsible for the development of tolerance to nicotine. Once tolerance has developed, a nicotine user must regularly supply the brain with nicotine in order to maintain normal brain functioning. If nicotine levels drop, the nicotine user will begin to feel uncomfortable withdrawal symptoms.
Taken from "Nicotine and the Brain" a NIDA article
So in other words, this means nicotine breaks neural paths, and then becomes them. As the nicotine breaks down, the connections are lost and more nicotine has to reach the brain to reconnect them. Withdrawal symptoms are the brain attempting to function without these connection. Over several days they will repair without continued nicotine consumption.
Nicotine is one of the few drugs that is truly addicting. Most other drug addiction are either a means of escaping comedowns or hangovers, or to reverse the depression that results of a lack of neurotransmitters. These other addiction can be beaten if a user has the will not to continually redose themselves. Nicotine on the other hand creates a physical craving and emotional backlash no metter how willing the user is to quit.
On top of this, once nicotine destroys certain pathways it loses most of its stimulant euphoria until those pathways can repair themselves.
--Jspeedy 19:38, 19 December 2005 (UTC)
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