Actions Of Nicotine On Brain Neurotransmitter Systems example essay topic
The chemicals empirical formula, C 10 Hl 4 N 2 was determined in the 1840's, and nicotine was synthesized in the 1890's. Nicotines systematic name is 3- (1-methyl-2-pyrrolidinyl) pyridine. Together with caffeine and strychnine, nicotine belongs to a group of chemical compounds called pyrrolidine alkaloids. Theyre bitter-tasting, often poisonous substances that are made by plants to discourage animals from eating them. Nicotine is a liquid alkaloid which can be obtained from the dried leaves of the tobacco plant, primarily found in a combined form of malate or citrate. One cigarette contains approximately 1.2 milligrams of nicotine, which, if injected in pure form, is as toxic as hydrogen cyanide, and could kill seven adults.
When you smoke, however, you get an extremely diluted dose, about 1 billionth of the nicotine content quoted on the cigarette packet. Nicotine has an extremely short half life in the body. Within forty minutes it loses about half its strength and the smoker feels the need for another cigarette. Nicotine has a powerful addicting effect because it is absorbed rapidly into the pulmonary circulation following inhalation from which it passes through the left side of the heart and into the cerebral circulation. It rapidly crosses the blood-brain barrier and binds to specific receptors in various parts of the brain. Stimulation of receptors by nicotine results in the activation of a number of neuro humoral pathways leading to release of acetylcholine, norepinephrine, dopamine, serotonin, vasopressin and various hormones.
Nicotine causes the release of the substance b-endorphin, an endogenous peptide that also binds to opiate receptors. This indicates a link between addiction to opiates, such as morphine and heroin, and addiction to nicotine. Nicotine affects nearly all components of the endocrine and neuroendocrine systems, including catecholamines, serotonin, corticosteroids and pituitary hormones. Some of these endocrine effects are mediated by actions of nicotine on brain neurotransmitter systems.
In addition, nicotine causes skeletal muscle relaxation and has cardiovascular effects. Nicotine is a powerful substance in controlling brain function. It interacts with specific receptors in brain tissue, and initiates metabolic and electrical activity in the brain. The individual cells within the brain, the neurons, release a whole array of chemical signals in communication with one another. The most common chemical signal that is used in the brain is a transmitter called glutamate, which stimulates the brain. The production of glutamate requires the brain chemical acetylcholine, and studies have shown that nicotine has similar affects to acetylcholine on the receptors in the brain due to their common dimensions.
How nicotine acts depends on factors including the amount of nicotine in the body, the time passed since the last cigarette and stress level of the smoker. Nicotine has a stimulating effect, but intake of larger doses can lead to paralysis, vasoconstriction and tachycardia. Nicotine mimics a chemical that controls heart rate. At blood levels of nicotine achieved by average smokers, stimulation of the central nervous system ultimately results in discharge of sympathetic neurons leading to an increase in blood pressure and heart rate.
These changes may be directly or indirectly related to the demonstrated associations of cigarette smoking with heart attacks, worsening of hypertension and stroke. Researchers realised that nicotine manipulates the mind on many different levels, and consequently conceived that in some way nicotine may even boost concentration, or improve memory. After smoking cigarettes, smokers perform better on some cognitive tasks than they do when deprived of cigarettes or nicotine. However, nicotine intake does not improve general learning. Nicotine is a sympathy-mimetic drug, similar to cocaine and amphetamines, stimulating the sympathetic nervous system.
Interestingly, scientists have begun to realise that nicotine may be of use as a medicine, as a treatment for various kinds of memory problems such as senile dementia. It may help with Alzheimer's disease and with motor tremors, a symptom of Parkinson's disease. Research has been conducted to observe the effects of nicotine on rats, specifically focussing on the effect nicotine has on memory. Nicotines mimicking of the brain chemical acetylcholine may explain why very few smokers develop Alzheimer's disease. In Alzheimer's disease there is an unusually low number of acetylcholine receptors, which may substantiate the theory that good memory depends on having sufficient supplies of acetylcholine. It has also been observed that people with schizophrenia and severe depression smoke much more than average, maintaining that smoking alleviates their symptoms.
This could certainly be true, as nicotine prompts the release of the powerful brain chemicals serotonin and dopamine, the very chemicals that are out of balance in these people. Nicotine has an adverse effect on the growth of a baby in utero and causes increased mortality during the delivery, increased incidence of brain damage, learning disabilities, Sudden Infant Death Syndrome and Attention Deficit Disorder. Ironically, prenatal exposure to nicotine may result in the newborn having an attention deficit problem, while nicotine is used as a primary treatment for Attention Deficit Disorder. Sudden Infant Death is triggered by a period of asphyxia during sleep.
Normally the brains respiratory centre will detect the plummeting oxygen levels and make the baby breathe deeper while at the same time, a rush of adrenalin makes the heart beat faster. Prenatal exposure to nicotine, however, may affect these survival systems and the baby may simply suffocate. Nicotine is called a neuro-teratogen, that is it damages the developing brain. Nicotine causes the absence of neurons (which enable us to think and act) in certain parts of the brain. It also causes functional damage where the nerve cells dont work properly. They are either incorrectly wired up, or they are quiescent where they should be active.
In an ordinary developing brain, acetylcholine flows from the neuron to its target cell, while a cholinergic neuron produces acetylcholine. Some of its target cells contain a specific receptor protein called a nicotinic cholinergic receptor, which responds to nicotine and acetylcholine. By depolarizing these target cells, nicotine tells that cell to stop dividing. This is particularly important in the nervous system because once nerve cells make the decision to stop dividing, they can never divide again. Nicotine causes this crucial step in brain development to occur prematurely due to its mimicking effect of acetylcholine. It also appears that females (both humans and animals) are more sensitive to the actions of nicotine than males.
This suggests that there are differences between the male and female brain, which is extremely interesting in the development of science. Studies have also proven that there is a relationship between nicotine and stress. We know that economic stress, psychological stress, social stress and physical stress can often lead to increased drug use, especially alcohol and tobacco. Stress increases cigarette consumption among smokers as they attempt to use nicotine as a relaxant. Furthermore, stress has been identified as a contributing factor in the initiation of smoking in adolescents. From studies conducted, it is also apparent that nicotine has an effect on body weight.
On average, cigarette smokers weigh approximately three kilograms less than nonsmokers. Many believe these smokers often use the physical act of smoking as a substitute for eating, but extensive research has shown a biological link between nicotine and body weight. Evidence of this is that many smokers who quit smoking gain weight. Nicotine also affects levels of insulin, the hormone that regulates glucose, affecting the smokers preference for sweet-tasting foods by changing the chemistry in the brain.
Nicotine also affects the brain chemical serotonin, which is believed to influence the consumption of carbohydrates. Scientists are currently working to develop a nicotine-like drug that controls body weight without causing addiction. This may play a role in reducing smoking in adolescent females who may smoke to reduce body weight. In a society where the majority of teenage girls are image and weight conscious, it is not surprising that a larger proportion of females appear to be smoking at parties, social gatherings and in day to day life. Nicotine Patches and gum are substitutes for cigarettes to help smokers overcome their addiction to nicotine. The primary problem is these products release nicotine slowly.
When you smoke a cigarette, you get a burst of nicotine that goes straight to the brain, where the pleasure chemicals dopamine and serotonin are released. This is the reason why many smokers find that nicotine patches and gum are not appropriate substitutes for cigarettes. Nicotine is a highly accessible, legalized drug and has similar addictive qualities to illicit drugs like heroin and cocaine. It is in fact more harmful than marijuana which is also illegal. I think nicotine is an extremely important drug which has a huge potential to be developed and refined for use in medical treatment.
I believe that research efforts should continue to focus on the importance of separating the nicotine from its dangers, including problems such as Sudden Infant Death Syndrome, Attention Deficit Disorder and adverse effects on babies in utero, to create a product which can boost concentration, improve memory and control body weight, as well as alleviating the symptoms of Alzheimer's and Parkinson's Disease sufferers. Although nicotine has created the problem of addiction in cigarettes, if we can separate it from its dangers, we may have a drug that is of great value to humans. 1640 Words Dulbecco, R (ed.) 1991, Encyclopaedia of Human Biology, Academic Press, Sydney. Kroschwitz, J & Howe-Grant, M (ed.) 1995, Encyclopaedia of Chemical Technology, John Wiley and Sons, Brisbane. J. Elks, J & Ganellin, C.R. (ed.) 1990, Dictionary of Drugs, Chapman and Hall, Melbourne. James Swan brick, J and James C. Boylan, J.C. (ed.) 1994, Encyclopaedia of Pharmaceutical Technology, Marcel Dekker Press, New York. Burch field, G et. al.
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