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Drugs In The Brain - With A Free Essay Review
K. Pierce; Professor Canby; Literature 3304; 20 June 2012
Drugs in the Brain
The effects of different drugs on the cells of the brain are tools that unlock information to how the brain works. Each type of drug has a different process of resulting effects that changes the molecular network of neuronal communication, this changes how the brain communicates with the rest of the body and the psychological mind. Neurons behave in a way where an external ligand can interact rather easily once it has made the journey to the nervous system. A ligand can bind to a neuron’s receptor and generate an entire sequence of events to take place within a cell. These sequences interact upon other mechanisms that ultimately affect the body in either positive or negative ways. The ways the body is affected is related to mechanisms of addiction and abuse of drugs, the more a drug is administered to a neuron the more tolerance it develops. When a drug is withheld from the cell, the cell reacts adversely causing withdrawal symptoms. Treatment and recovery are possible but it takes longer for a neuron to regress a learned behavior, known as neural plasticity. The behavior of neurons explains how drugs affect the brain in such different and possible adverse ways.
Neurons are the cells of the nervous system in living organisms. There are billions of neurons in the brain alone, which all communicate with each other and influencing the body’s everyday functions and behaviors. All neurons have four defined regions that contribute to the ability to communicate with other neurons and psychoactive drugs can exert effects within these regions (Ksir, Hart and Ray 85). These regions include the cell body, dendrites, axon, and presynaptic terminals. The cell body holds all the nucleus and other organelles common universally in all cells. The dendrites extends from the cell body towards other neurons, within the membrane of the dendrites are “specialized structures that recognize and respond to specific chemical signals” (85). These structures, known as receptors, are the site of a drugs specific interaction. The axon also extends away from the cell body to interact with other neurons, “and is the main conducting unit for carrying signals to other neurons” (Kandel, Jessell and Schwartz 21). The signal in which the axon carries is called the action potential, an electric all-or-none pulse. The action potential travels down to the end of the axon to the presynaptic terminals, which stores “chemical messengers” called neurotransmitters (Ksir, Hart and Ray 85). The action potential electric charge into the terminal allows for the cells membrane to permit the entrance of ions. The flow of ions changes the voltage of the terminal which signals the release of the neurotransmitters to go interact with other neuron’s receptors. These terminals are another site of interaction for drugs, either by altering the physical properties of the cell by blockage or increasing the amount of transmitter released onto a receptor.
There are many different types of neurotransmitters with numerous chemical pathways they take to initiate different effects on the brain. The main neurotransmitters that are associated with different exogenous drugs “include dopamine, acetylcholine, norepinephrine, serotonin, GABA, glutamate, and the endorphins” (91). These neurotransmitters have different chemical pathways that constitute one physical structure in the brain to another structure in the brain. A pathway for dopamine is the mesolimbic dopamine pathway, and is proposed to be the main component responsible for the “reward” properties (91). Many stimulant drugs effect the neurons that release dopamine by indirectly changing how much or how long the transmitters are active. Neurons that release acetylcholine fall into cholinergic pathway associated with motivation and reward, sleep and arousal, cognitive processes and may involve some pain reception (Iversen, Iversen and Bloom 135). Pathways that release norepinephrine are vast and travel all around the brain. This neurotransmitter influences the level of arousal and attentiveness, as well as controlling the complex system of energy balance and body weight. It is possible that through these norepinephrine pathways that stimulant drugs induce wakefulness (Ksir, Hart and Ray 91-92). A low dose of amphetamine is an example of a stimulant that promotes wakefulness and decreased fatigue. There are many different types of serotonergic neurons and pathways throughout the brain and are involved in a vast array of functions such as aggression, depression, eating behaviors, sleep and many more. One type of serotonin receptor can produce hallucinogenic and other odd behaviors when acted on by LSD, which acts as a partial agonist (Iversen, Iversen and Bloom 486). The neurotransmitter GABA exerts an inhibitory function and “many sedative drugs act by enhancing GABA inhibition (Ksir, Hart and Ray 92). An example of a drug that acts on GABAnergic neurons is alcohol. Ethanol enhances the release of GABA, which stimulates the uptake of chlorine (a negative charged ion), decreasing the voltage of the neuron. A decreased voltage makes it harder for action potentials to generate, leading to disinhibition and sedation (Iversen, Iversen and Bloom 510). Contrary to GABA, glutamate is an excitatory neurotransmitter and “that specific glutamate pathways may be important for the expression of some psychoactive drug effects” (Ksir, Hart and Ray 92). Endorphins are neurotransmitters that play a major role in pain relief and can be stimulated endogenously or exogenously with drugs such as morphine (92). Exogenous ligands or drugs affect the “availability of the neurotransmitter in the synapse”, either the amount of transmitter released or how long it remains in effect. A drug can also apply is effects “directly to the receptors”. This is possible when the drugs structural conformation is very similar to the endogenous neurotransmitter, therefore, it can “mimic the action” of the transmitter (96).
The first step in a drug interaction with a neuron’s receptor or presynaptic terminal is journey the drug molecules take to get to the brain. “All psychoactive drugs reach the brain tissue by way of the bloodstream” and are taken by one of the three major routes of administration: by mouth, injection, or inhalation (113). Taking a drug by mouth is by far the simplest way to take a drug but is the most complex for the actual drug molecules to enter the bloodstream. The ligand has to be able to withstand stomach acid, absorption from the gut, as well as metabolizing through the liver. Consequently only a small portion of the drug actually enters the bloodstream (113-115). A faster way for a drug to get into the bloodstream is to inject directly into a blood vessel, IV injections also make it easier to deliver high concentrations of a drug without the stomach problems associated with ingesting such ligands. Injecting drugs intramuscularly is an even faster at absorbing into the bloodstream because of the higher blood supply in muscles. This is the reason why patients get shots and vaccines in the arm versus other injectable sites (115-116). The last common route of administration is inhalation, a common drug delivery system used from smoking. Inhaling a drug is a very efficient way to deliver a drug to the blood stream because of the intense supply of capillary walls. Therefore, the drug enters the blood stream rather rapid resulting in quicker results. “The blood leaving the lungs moves fairly directly to the brain, taking only five to eight seconds to do so”, while blood from the vein has to detour to the heart first before heading to the brain (116). This makes smoking a psychoactive drug a more desirable way to administer a drug. Once a certain amount of drug molecules are in the blood stream, the affinity of a specific drug relates proportionally how fast the drug will absorb through the capillary walls. Only very few molecules will pass the blood-brain-barrier to enter the brain and actually interact with the central nervous system’s neurons.
The use of many of drugs, addiction is a very probable cause. There are certain areas in the brain that are theoretically more important for the mechanisms of addiction. The nucleus accumbens is one of the more important areas in the brain mediating motivation and reward and those producing behavioral output. Another element in the theory of addiction is the mechanisms of learning and memory. Addictive drugs have the ability to take over these mechanisms and adverse learning patterns are formed. As the addictive process develops, control is lost and behavior known to be controlled normally by the ventral stratum is controlled by the dopamine system of the dorsal. This plasticity in the brain is why relapse is so common and hard to overcome (Iversen, Iversen and Bloom 439-440). Treatments are available for many types of addiction; the neurons changed by the abuse of certain drugs react adversely to treatment methods.
Throughout history drugs have been used to explore the link between brain and behavior functions. Exogenous ligands of any sort affect the neuronal process of the brain that in turn affect the moods and behaviors of the subject. Very little of the ingested or injected drug actually makes it to and through the blood brain barrier to enter the brain and actually have cellular effects of neurons. Many drugs that increase neurotransmitter release are used in healthy clinical situations such as anti-depression medications that increase serotonin release on very specific 5-HT receptors. While other drugs block the reuptake or increase the amount of the neurotransmitter dopamine to eventually lead to addiction and tolerance. The treatment options that are available are relatively harsh because of new methods of learned behaviors must be acquired to completely be cured.
It is not often on this site that I am introduced to new words, but you've introduced me to a bundle, including "serotonergic" which ought to have figurative applications beyond its usage among people who have a sworn a sacred oath to write like automatons.
(Assignment: Write a poem entitled "The Serotonergic Caress." It should also include the word "excitatory" -- a word I've come across before, but never in a poem, which is pity. There is a whole new world of (probably unreadable) poetry waiting to be conquered by medical scientists.)
All of the foregoing is of course no more than a fairly transparent attempt to delay the inevitable admission that I have not much to say about your essay beyond the fact that it seems a rather desultory list of relatively obscure facts articulated with what looks like either a precise command of the relevant vocabulary, or a good imitation of such command (I don't have the time to do the work that would be needed to allow me to judge such matters). If your intention was to marshal these facts in the service of an argument about the nature of drug addiction, and the problems affecting its treatment (which is the closest thing that you have to an argument here), then a good deal more work needs to be done to improve the organization and clarity of that argument. (A thesis would help. Transitions between paragraphs that serve as guideposts that explicitly inform the reader about the progression of the argument would help. Establishing more explicit links between the factual information presented and the claims made about drug addiction would help.) But if the purpose of the essay is simply to offer a general discussion of "drugs in the brain," then perhaps none of that is necessary (although even scientific literature - perhaps especially such literature - values obvious organizational cues, in the form of transitions or subheadings).
There are several typographical errors, which I leave you to hunt down (that's a pedagogical decision, honest!). You use commas often to splice independent clauses. Your second sentence is an example; there are several others. Try to avoid such comma splices; you can use a semicolon to separate such clauses, as I have just done. And of course you can also use a period.