Psychology 321: Biological Bases of Behavior
First Project
An in depth review of the drug Methelynedioxymethamphetamine,
(MDMA or "Ecstacy")
The Chemestry of MDMA: Jennifer McNeil
Many people have thought that 3,4-methylenedioxymethamphetamine (MDMA), also known as Ecstasy, is a combination of several illicit drugs, such as cocaine and heroin, however, there is only one chemical configuration represented. However, this belief is false. MDMA has it's own chemical makeup and the process of synthesis does not include other illicit substances (Cohen, pp 12-14). MDMA is derived from the oils of plants such as nutmeg, sassafras, saffron, dill, parsley seed, crocus, vanilla beans, and calamus. However, the chemical process of synthesis is much more complex than just extracting oils from plants (Taylor).
The synthesis of MDMA has four processes: 1. extraction of safrole from sassafras oil, or other sources (piperonal), 2. Isomerization of safrole into isosafrole by heating with NaOH or KOH, 3. Oxidizing isosafrole into MDP-2-P, and 4. Using the Leukart Reaction add N-methyl-N-forumyl-MDA to MDP-2-P resulting in MDMA (Taylor). Figure 1 gives the chemical structure and outline of the synthesis of MDMA.
MDMA Synthesis
"MDMA is an amphetamine derivative that is related chemically to both amphetamines and hallucinogens" with neurotoxic effects (Elk, p 349). It has also been termed as an entactogen, which is a substance described as "producing a feeling in one's innermost being" (Medical Information). There are many features of MDMA that set it apart from other drugs of its kind, although it MDMA has been classified as a "hallucinogenic-amphetamine," it does not have the potent stimulant and hallucinogenic effects. As a 3,4 disubstituted amphetamine, it is the only substituted amphetamine that only has substituted patterns in the 3 and 4 positions. Another unique feature is that it is "a secondary amine, with the basic nitrogen being substituted with an N-methyl. These attributes separate MDMA from the hallucinogenic and amphetamine agents that are the most potent of the primary amines. Another feature distinguishing MDMA from the hallucinogens is that the R-entantiomer of hallucinogens is the most potent agent in the Central Nervous System (CNS), whereas the R-form of MDMA is the least potent (Cohen, pp15-17). .
The Route of Access of MDMA: Jennifer McNeil
MDMA's most popular route of access is through oral ingestion. Although, it can be administered through intravenous injection, smoking or snorting it, and very rarely through suppository. When MDMA is swallowed it gets digested in the stomach where it enters the blood stream. Approximately 20% reaches the brain, two thirds is eliminated, unchanged, through urine, and 7% is "metabolised" into MDA (E is for Ecstasy). Once MDMA enters the brain it reacts with the chemicals in the brain, leading to the effects felt by MDMA.
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3 types of MDMA Tablets (copyright erowid.org)
Neurotransmitters Involved: Rachel Anthony
The various chemicals in the brain called "neurotransmitters" are responsible for adjusting our mood and activity level to suit different situations. Serotonin (5-Hydrotryptophan) is one common neurotransmitter well known for the large role it plays in the regulation of mood, heart rate, sleep, appetite, pain and more (Carlson). MDMA, or ecstasy, causes large amounts of serotonin to be released and stored in the terminal boutons of an axon, which is responsible for the primary effects of MDMA (Cohen, p.19). This is because MDMA has a greater affinity for the uptake transporters than serotonin, so MDMA will generally enter the axon terminal first. Normally, serotonin is synthesized and stored in the synaptic vesicles, where it is released into the synaptic cleft in response to an electrical charge that is sent down the axon. The serotonin molecules float around and into serotonin receptors and reuptake transporters (or synaptic membrane serotonin transporters) on the dendrite of another neuron (Granquist, p.1). The serotonin molecule causes the receptor to send chemical information down the dendrite to the cell body of the neuron; the reuptake transporter takes the serotonin back from the synapse where it is once again stored in the synaptic vesicles (Granquist, p.1).
A view of the vesicle releasing serotonin into the
synapseduring normal chemical reactions
(without the addition of MDMA/ecstasy).
MDMA, however, causes the serotonin neurons to synthesize and react differently than normal. MDMA causes the synaptic vesicles to release enormous amounts of serotonin into the synaptic cleft (Sferios, p.6). In addition, MDMA blocks the reuptake of serotonin similar to the way in which anti-depressant drugs such as Prozac, sertraline and paroxetine do (Granquist, p.1). These drugs are serotonin specific reuptake inhibiting (SSRI) drugs. However, unlike these drugs, serotonin is thought to enter the neuron directly through the reuptake transporter, and once again release serotonin into the synaptic cleft through the serotonin transporter (Sferios, p.13).
A view of the vesicle releasing serotonin into the synapse
during the peak experience of taking MDMA/ecstasy
(about one hour after the onset of the drug).
Hours and hors after taking MDMA, the serotonin reuptake transporters will remove most of the serotonin molecules from the synapse, and the effects caused by the MDMA will start to decrease (Sferios, p.14). At this point, "monoamine oxidase", an enzyme that breaks down serotonin, comes into effect by breaking down most of the serotonin left that the reuptake transporters have removed and are still removing (Sferios, p.14). At this same point in time, about four hours after taking MDMA, the serotonin that the brain has produced is used up. MDMA releases and depletes the serotonin that the brain has already produced, so taking more MDMA will not cause more serotonin to be created.
The brain can take up to two weeks to replenish serotonin levels so they are back to normal, and the larger the dose of MDMA, the more serotonin is depleted, and the longer it takes to replenish (Sferios, p.16). The prolonged effects of MDMA (twenty four hours to one week after use) can cause more significant damage to the serotonin nerve terminals and a substantial loss of serotonin reuptake transporters (Cohen, p.19). Often, these degenerative effects on serotonin nerves have been irreversible because MDMA alters neurotransmitter functioning and monoamine levels in specific regions and depending on dosage after treatment (Cohen, p.20).
Although the neurotransmitter most involved in the effects of MDMA is serotonin, MDMA also causes dopamine to be released from dopamine cells. This dopamine also plays a role in neurotoxic damage caused by MDMA. This damage is currently believed to occur from the results of testing on laboratory animals. After MDMA causes a serotonin depletion, reuptake transporters are left empty (Sferios, p.19). This causes dopamine to enter the reuptake transporter and get transferred into the serotonin axon where it is extremely toxic and should not be (Sferios, p.19). Furthermore, monoamine oxidase breaks the dopamine down into hydrogen peroxide, also very toxic to the cell, and oxidizes the cell (or breaks it down with oxygen) which is not normally oxidized (Sferios, p.19). Dopamine, on the whole, causes a serotonin axon terminal to become "shriveled up" and damaged. As with most drugs, the effect of MDMA on the neurotransmitters in the brain varies depending on the user and the dosage.
Part of the Neuron Affected: Erin Misoni
The part of the brain that is most affected by MDMA are the serotonin-producing neurons. Through much animal research with MDMA it has been found that this drug significantly damages serotonin-producing neurons in the brain. Serotonin is a major neurotransmitter, or chemical messenger, in the brain that influences mood, appetite, sleep, and other important functions.
Once MDMA is taken into the body the initial effects produce heightened levels of serotonin in the brain. Following these discharges of serotonin, ongoing synthesis has shown to be inhibited. After 3 to 6 hours noticeable reductions in brain serotonin concentrations can be found. These initiatory effects appear to produce changes in serotonin that are luckily reversible (Cohen, 19). In the second stage (twenty-four hours to one week), the prolonged effects of MDMA become more apparent, with significant damage to serotonin nerve terminals characterized by substantial loss of serotonin reuptake sites. These degenerative effects on serotonergic neurons are known to be irreversible (Cohen, 20).
Studies have demonstrated that MDMA alters neurotransmitter functioning and causes drastic neurodegenerative effects on serotonergic function. Following treatment monoamine levels have been shown to be altered in a region-specific and dose-dependent manner. MDMA also causes neurodegeneration of serotonergic uptake sites, as well as marked reductions in the activity of tryplophan hydroxylase, the rate limiting enzyme of serotonin synthesis (Cohen, 20).
Studies have revealed that MDMA is neurotoxic to serotonergric nerve fibers in rats, mice, guinea pigs, and monkeys (Cohen, 20). Dr. George Ricaurte, a scientist at the Johns Hopkins Medical Institution found that 12 to 18 months after the brains of squirrel monkeys had been damaged by MDMA, serotonin-producing nerve fibers had regrown abnormally in some regions as well as failing to regrow at all others (Mathias, 1). "MDMA selectively damages serotonin neurons in virtually all species to date," Dr. Ricaurte says (Mathias, 1).
During the long-term study with the squirrel monkeys, some brain areas, those containing structures involved in memory and learning, damaged neurons failed to recover. However, in other brain areas, particularly those areas involved in regulating sleep and appetite, those damaged neurons regrew nerve fiber excessively, resulting in too much serotonin being released. "This means that when we evaluate humans previously exposed to high doses of MDMA, we should be looking for less of serotonin function in some regions, but perhaps normal or increased serotonin function in other regions," Dr. Ricaurte says (Mathias, 2).
Dr. Ricaurte's studies have found that MDMA damages serotonin-producing neurons in the brains of nonhuman primates. The illustration shows a normal neuron. The shaded area in the middle illustration shows the axon terminals of the neuron that are damaged by MDMA. The illustration on the right shows how, 12 to 18 months after being damaged by MDMA, serotonin-producing nerve fibers have regrown excessively in some areas and not at all in others (Mathias, 1).
A decade of research has shown MDMA causes a deficit of brain serotonin in every animal species, but what about in the human species? Just recently, several strands of evidence have indicated that similar deficits occur in people (Morris, 1). Some researchers whom wanted to investigate the status of brain 5-HT neurons in MDMA users conducted a experiment, and their results were surprising. Their findings are as followed: " In summary, our data suggest that people who use MDMA as a recreational drug are unwittingly putting themselves at risk of developing brain 5-HT neural injury. In addition, systematic studies of MDMA-exposed individuals with highly selective brain 5-HT transporter deficits may give important insights into the functional role of brain 5-HT in human behavior. Potential functional consequences of MDMA-induced brain 5-HT neurotoxic lesions are not yet clear, but may include depression, anxiety, memory disturbance, and other neuropsychiatric disorders in which brain 5-HT has been implicated"(McCann, 8). These findings prove that MDMA has the same effect on human serotonergic neurons as it does on animal's serotonergic neurons.
In some research MDMA not only proves to damage serotonergic neurons, but also to decrease the concentrations of cerebrospinal fluid 5-hydroxindoleacetic acid (5-HIAA) the primary serotonin metabolite. Significant decreases in concentrations of 5-HIAA have consistently been found in laboratory animals following the administration of the drug. One study found concentrations of 5-HIAA in human cerebrospinal fluid to be greatly reduced in individuals who have had prior exposure to MDMA (Morris, 5). However, a different study, did not find MDMA users to have decreased levels of 5-HIAA (McCann, 9).
To conclude, the long term use of MDMA causes some serious damage to the serotonin producing neurons of the brain. This long term use results in permanent damage to neurons in some areas of the brain (memory and learning), and the excessive regrowth of damaged neuron nerve fibers in other areas of the brain (sleep and appetite) (Mathias, 2). In the beginning various experiments on animals found this statement to be true, and as scientists have progressed in their research they have found that MDMA also affects the serotonergic neurons in humans (Morris, 1). Other research has suggested that MDMA decreases concentrations of cerebrospinal fluid 5-hydroxindoleacetric acid, but not enough research has been done to support this theory (Morris, 5).
Inhibitory or Exitatory potential changes: Bobby Carethers
The excitatory and inhibitory processes that influence behavior when we ingest drugs are not fully understood. MDMA is a neuro-toxic drug that effects specific serotonin sites within the brain. MDMA is primarily an excitatory drug that depletes the brain of serotonin. The neuropharmacology in animals is different. In monkey and rodents 5ht is mostly produced in the hippocampus. (Lancet, p1433) This has a very large effect on sleep and other mood factors. Research on primates' serves as the best predictor of human behavior.
Once MDMA enters the brain area it triggers with the brains receptors. This causes presynaptic phenomenon. When we ingest MDMA it mimic normal chemical action. MDMA manipulates brain neurons as an agonist or an antagonist or a partial agonist. All drug effect serotonin but MDMA is unique. It is known to effect several types of serotonin receptors. Subtypes like 5HT-1A, 5HT-1B, 5HT1E, 5HTIF, 5HT2A, 5HT2C, 5HT3, 5HT4, 5HT5, 5HT6 and 5HT7. These receptors are located in nine parts of the brain, mostly in clusters (Carlson 1998) There are several sub types because a different receptor is involved with a different neuron effecting mood or other factors. MDMA binds with the cell as an agonist. This causes the cell to produce postsynaptic potentials effecting behavior. These potentials could produce a higher heart beat or sexual arousal. This is a direct reflection of dopamine that is released. This is a common drug within the brain that effects inhibitory and excitatory processes. The second effect on receptors is the partial agonist; this causes the cell to release transmitter substance slowly. This could have an effect in slowing the body's reflexes. This could explain the euphoria or closeness that a person feels. The third effect on the receptor is called the direct antagonist this causes total inhibition of the cell. This prevents the normal flow pattern of brain activity. This presynaptic phenomenon can not assist the calcium channels to open or activate the presynaptic heteroceptors. After MDMA releases serotonin and dopamine the postsynaptic receptors trigger the reuptake of the serotonin and the dopamine. This does not happen for a long time. These effects last about 4 to 6hours. The presynaptic neuron reabsorbs and recycles the molecules of the neurotransmitter that it has previously secreted in conveying an impulse to another neuron. In addition monoamine oxidase enzyme tries to destroy as much serotonin and dopamine as possible. This process is nearly impossible because MDMA inhibits this process to. The inhibition of serotonin causes any individual to experience severe anxiety and depression.
Ion Channels Effected by MDMA: Rachel Chappelear
Ecstasy, MDMA, or 3,4 methylenedioxyamphetamine obtains it's effects from its interaction with serotonergic neurons in the brain. These are neurons that produce serotonin, (5-HT), one of the monoamines, a neurotransmitter substance that is responsible for many of our psychological states such as mood, sleep, arousal, appetite, and regulation of pain. MDMA has been shown to significantly damage the serotonergic neurons and effects ion channels of this neuron during a process that blocks the reuptake of serotonin. This process will be explained in greater detail and a general overview of the serotonergic neuron will be given and are the focus of this report.
As mentioned above, serotonin is produced by neurons and influence many psychological states. It is made from the amino acid tryptophan (we can get this from eating turkey!). A hydroxyl group is added to tryptophan by the enzyme tryptophan hydroxylase to make 5 hydroxytryptophan or 5 HTP. Another enzyme, 5 HTP decarboxylase, removes a carboxyl group from 5 HTP, making serotonin or 5 HT. "Some 5 HT is present in the cytoplasm of serotonergic cell bodies and nerve terminals but most of the neurotransmitter is stored in vesicles....5 HT is
"accumulated in storage vesicles via a membrane transporter that appears to be identical to that found in [the other three monoamines] "(Feldman, Meyer, Quenzer, p. 352).
5 HT has many types of receptors. Some of these include 5 HT1A, 5 HT1B, 5 HT1D, 5 HT1E, 5 HT1F, 5 HT2A, 5 HT2B, 5 HT2C, and 5 H3. Some of these are autoreceptors on the presynaptic part of the neuron; 5 HT1B and 5 HT1D to be precise, and 5 HT1A is an autoreceptor located on the membrane of the dendrites and soma.
Some information is available concerning the mechanism of action of 5 HT autoreceptors. Stimulation of somatodendritic autoreceptors has been reported to inhibit firing by hyperpolarizing the cell, probably throughout an increase of membrane potassium (K+) conductants...In contrast, presynaptic autoreceptors do not alter impulse transmission, but rather inhibit some aspect of stimulated secretion coupling of transmitter release. Gothert (1980) hypothesized that presynaptic 5 HT autoreceptors operate by modifying the influx of Ca+2 through voltage dependent Ca+2 channels. Cyclic AMP may also play a role in this process, as both 5 HT1B and 5 HT1D receptors have been transported to inhibit the activity of adenylylcyclase. Differences in the mechanisms needed to modulate impulse flow and transmitter release may help to explain why distinct 5 HT receptor subtypes are required for these purposes (Feldman, Meyer, and Quenzer, p. 354).
Termination of the effects of synaptically released 5 HT occurs largely by means of a reuptake process that presumably allows at least some of the transmitter to be recycled for further use. Uptake is mediated by a transporter protein found in the plasma membrane of serotonergic neurons. The uptake process displays saturability, a high affinity for 5 HT, a Na+ dependence, and a requirement for metabolic energy...as would be expected for a carrier mediated mechanism (as opposed to simple diffusion). 5 HT uptake also shows structural specificity and can be selectively inhibited by a number of different drugs (Feldman, Meyer, and Quinzer, p. 355)
This is where MDMA is tied in with the overview of the serotonergic neuron. It has been proven that MDMA is one of the drugs that block or inhibit the reuptake of 5 HT.
By inhibiting the reuptake of serotonin MDMA causes the release of serotonin. "MDMA appears to enter the neuron either through passive diffusion or directly through the reuptake transporter, and causes the release of 5 HT. This release is calcium independent...and appears to come from cytoplasmic stores rather than from synaptic vesicles. The released 5 HT then enters the synaptic cleft through the 5 HT transporter"(Granquist, p. 1). To better understand the process involved with, or the ion channels effected by MDMA, a brief overview of serotonin transport across the plasma membrane shall be explained.
The driving force for transport is the Na + electrochemical gradient across the membrane....Na + binds to the carrier protein, followed by 5HT...Although chloride (Cl-) ions are not required for 5 HT binding, they are necessary for net transport to occur. After translocation of the carrier in the cell membrane, 5 HT and the cotransported ions dissociate from the respective binding sites. Potassium then binds to the carrier, leading to translocation of the binding complex back to the exterior of the membrane, where the cycle can repeat. Most researchers currently believe that uptake inhibiting drugs bind to the same site on the transport complex as 5 HT itself (Feldman, Meyer, and Quenzer, p. 355).
MDMA's psychedelic effect may come from it's interaction with the 5 HT2 receptor which has agonist properties (involved in stimulation rather than blocking) that are found to be associated with other psychedelic drugs such as LSD.(Granquist, p. 1)
In summary, ecstasy or MDMA directly effects the ion channels involved in serotonin reuptake and its release. This action with serotonin may be because of ecstasy's psychedelic effects including hallucination, feelings of euphoria, emotional connection with others, and sensual overtones. Ecstasy does, however, damage the seotonin neuron, as was discussed in the report on MDMA's effects on neuron parts. This damage may cause adverse effects on serotonin related functions such as mood, sleep cycles, and aggression. The information given by this report should help potential users decide whether the short term positive effects outweigh long term damage to serotonergic neurons.
Physiological Changes: Jamie Stuart
The physiological effects that methylenedioxymethamphetamine (MDMA) produce can vary immensely in each individual under its influence. Just as the behavioral changes can depend largely on the person experiencing the MDMA, the physiological effects can occur at random.
When taken orally the physiological effects of MDMA, (which are more amphetamine-like), can begin to occur within 30-45 minutes. In a neuropsychopharmacology sense, the mechanism of action taken by MDMA is a facilitation of synaptic release, a release of Dopamine, and a blockage of Dopamine reuptake transporters. The major effect in result is a sympathomimetic response (Feldman 178). The detailed result is an extensive list of short term (in most cases) effects, not limited to, but including: headache, high blood pressure, nausea, vomiting, rapid heart beat, trisma (clenching of the jaw), sweating, tremors, blurred vision, muscle spasms, backache, tongue and cheek chewing, bruxia (teeth grinding), dizziness, dryness of mouth, profound physical relaxation, nystagmus (eye wiggles); in extreme cases such as overdose: faintness, muscle cramping, seizures, loss of consciousness, and panic attacks. Death is also a possibility.
Each of these physiological responses can be damaging and produce long lasting effects. MDMA effects every inch of the human body. MDMA can be quite damaging to the circulatory system, due to elevated blood pressure and heart rate for long periods of time. An amphetamine abuser can take up to 15 times more than a maximum legitimately doctor prescribed dose. Blood pressure can increase to dangerous levels, sometimes causing blood vessels in the brain to burst. This can eventually lead to stroke. Kidney failure can occur as well as the death of large amounts of muscle tissue which can stop circulation, known medically as cardiovascular collapse (Tschirgi 1992).
Just as well, the physiological effects MDMA has on the brain is quite damaging. In the 1970's animal research involving MDMA began. The repeated administration of methamphetamine found persistently reduced Dopamine concentrations and tyrosine hydroxylase activity in the caudate nucleus (Feldman 566).
The blockage of Dopamine reuptake transporters, as mentioned before, can also lead to a total loss of the reuptake sites. This is due to the fact that MDMA acts as a Serotonin agonist and these agonist effects cause the damage to Serotonin nerve terminals and the loss of reuptake sites. Degeneration of nerve terminals for Serotonin has been demonstrated in rats, mice, guinea pigs, monkeys, and baboons (Levinthal).
The other long-term physiological effects from MDMA include:
Death has occurred on several different instances. This is the result of a physiological response gone unnoticed. Heat stroke is very common while under the influence of MDMA. Body temperature has risen and can tend to go unnoticed if the individual is not paying attention. The greatest risk to have heat stroke is within a person who has a fairly low level of the enzyme in the liver that breaks down MDMA. People with a high level of enzyme on the other hand suffer a greater risk of brain damage. The body's temperature is regulated by the serotonine system. The disturbances of the system that MDMA cause may lead to the regulation going haywire. This may lead to a traumatic effect on the body's muscle tissue. The muscle is dissolved and floats into the blood stream. Patients being hit with this response find it for example, hard to walk, because the muscles no longer are whole and strong enough. Via the blood stream muscle fibers enter the kidneys and thus there is also a risk that those will be taken out (Dagbladet 1996).
Another cause of possible death is a result from an exaggerated consumption of water. A common place of recreational MDMA use is at 'raves'. Or underground all night dance parties. A person experiencing the effects of MDMA will dance for lengthy periods of time at which point they will no longer pay attention to there body's need of replenishing itself. The person will then drink extraordinary amounts of water to "make up" for dancing for so long and being so hot. This is extremely dangerous. An excess of water can lead to water intoxication. This is a case in which water floods the body's cells causing cells to swell and then burst. Bodily functions shut down and the remaining water can get into the brain causing either brain damage or death.
Another danger that MDMA can inflict upon an individual's body is from MDMA's lessening of the awareness of pain. This is indeed a psychological and physiological problem. The MDMA gives the user the energy to do all sorts of activities such as dancing, hiking, climbing, etc. The person will not notice the pain their body is in if they are sustaining blisters, bruises, cuts, etc.
The immune system can be effected as well. MDMA users may experience a decreased resistance to disease. This is under speculation about whether or not this is from the pharmacological "body load" of MDMA, or the heightened activities that are involved with MDMA such as dancing and close contact with other people. Consequently, MDMA has a large physiological impact on the human body.
Primary Behavioral Changes: Gary Van Horn
When a person first uses MDMA (Methylenedioxymethamphetamine), or Ecstacy, they use it in order to achieve certain desirable effects which they believe will heighten their enjoyment of life for a certain period of time. Along with these cognitive changes they usually expect their behavior to change in some way which, hopefully, is conducive to their enjoyment of their drug experience. In the case of MDMA the average user not only behaves in a way conducive to the enjoyment of their experience but will often heighten the experience of the people who are using the drug around them as well creating a sort of reciprocal effect which incites further stimulation from all around the user. This is one reason that people who use MDMA will often take it in a small group of people that they trust, and with that group go out to a party or nightclub where they will feel free to let their inhibitions go while still feeling that they can return to their group in case of danger (Cohen, 1999). Another reason for taking the MDMA in a small group is that it seems to increase subjects understanding of other people and an increased level of openness or ability to interact with others which are effects that would perhaps be wasted on strangers whom one might not speak to again, but would be preserved by the lasting relationship changes caused in a group of friends (Cohen, 1999). Aside from being quite a bit more open than usual people who are under the influence of MDMA will appear energetic, excited, happy, and playful assuming they are feeling none of the negative effects of the drug (Elk, 1996).
Another behavioral effect of note is the decrease in violent behavior. Often many users of MDMA will congregate at large dance parties called raves and these types of parties are usually large, loud, and full of people who are under the influence of illicit substances. However, despite the size of these parties and the number of people involved, there is rarely any violence associated with them. This is perhaps due to the effects of MDMA on mood and aggressiveness. Out of a group of twenty MDMA users 80% reported a decreased level of defensiveness, 60% a decreased sense of separation from others, and 0% reported an increased level of aggression (Leister et al., 1992).
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A group of people dancing while under the influence of MDMA (from rave.stranger.com) |
Though all of the positive effects of MDMA seem as if they would promote sexual activity among users, most users do not report being any more promiscuous than usual while experiencing the effects of MDMA. This can perhaps be explained by data collected from users first-hand accounts of the drug experience which point to a decreased level of libido. Users do, however, report that they often have a need for intimacy which may make them appear hedonistic to some degree due to and increase in embracing and kissing of both friends and strangers (Elk, 1996).
Often users of MDMA will stay out all night at a party or rave, never tiring of the atmosphere or the physical exertion involved in dancing all night long. This seemingly tireless behavior can be explained by a combination of the effects of Ecstacy, one of which is to act as a stimulant. Add that to the heightened level of sensory perception and a desire to be in constant motion reported by many users and one can easily see why people who use Ecstacy usually stay up all night (Elk, 1996). This effect has been described as an "amphetamine-like rush" (Cohen, 1999) that occurs about 20 to 40 minutes after ingestion of a pill containing MDMA. Aside from these physical effects, however, there is also a cognitive aspect to this behavior. According to 18 users out of 20 surveyed, MDMA creates an altered perception of the passage of time. The users surveyed stated that it did not create an overall effect of slowing down or speeding up time, but rather that time was "compressed," "dilated," "expanded," "slowed down," and "sped up." Other users were simply aware that their perception of time was altered but could not say exactly how it had been altered (Leister et al., 1992). This altered perception of time coupled with a reported increased ability to interact with others provides just as much of an explanation as to the seemingly tireless behavior of Ecstacy users as MDMA's stimulant effects. This stimulant effect does not necessarily make the person more productive though, in fact users report a decreased desire and a decreased ability to perform mental or physical tasks. This phenomenon, which seems like an anomaly due to the tireless party behavior exhibited by so many Ecstacy users, can be explained by the fact that dancing or partying is usually not seen as a task, but rather the user is less likely to do something which is considered a task such as cleaning, cooking, or homework.
Unlike many other drug users only a little more than half of Ecstacy users report any change in their visual perception, and of those the most common accounts were of an intensification of visual imagery (Leister et al., 1992). This intensification of perceived images can cause a person who is under the influence of Ecstacy to appear as if they are completely absorbed by color and light. Although it may be hard to perceive whether a person is absorbed by imagery the idea that many people enjoy visual stimulation while on Ecstacy is proven, in a way, by the behavior of the people that run parties or raves who often fill the environment with bright colors, strobe lights, black lights, or any number of things which bombard visual senses.
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Picture of a person dancing at a rave with glow-sticks on their body (from rave.stranger.com) |
Adverse Behavioral Effects: Gary Van Horn
Most people who use Ecstacy report that they would do it again if they had the chance, which leads one to believe that the felt taking MDMA was a good experience overall, however a percentage of the population that has taken MDMA has stated that they would not take it again due to some type of adverse effects. One of the adverse effects that is most commonly reported is bruxism (or trismus), a condition more commonly referred to as uncontrollable clenching of the jaw. Though this effect has never been reported as causing damage to the teeth, or resulting in a permanently clenched jaw, some level of discomfort is derived from a long night of jaw clenching (Leister et al., 1992). Along with bruxism users often complain about experiencing lower backache, nausea, headaches, and blurred vision all of which are usually felt by the user approximately thirty minutes following ingestion and continue with decreasing intensity throughout the entire six to eight hour drug experience (Cohen, 1999). Another adverse effect which has been reported is vomiting, this effect, however, is not very common among Ecstacy users unless they have experienced an overdose of the drug (Leister et al., 1992). Along with vomiting users who overdose on MDMA may experience persistent insomnia, agitation, depression, psychosis, "rage reactions," hallucinations, over activity, and overstimulation of the heart which may result in death (Elk, 1996).
One adverse behavioral effect which is perhaps most common among users of MDMA is a severe mood depression following use of Ecstacy found by scores on the Beck Depression Inventory (BDI). Apparently most people who use MDMA on a certain day will experience a lowering of mood about three days later which is marked by an average score of 11.75 on the BDI (Curran and Travill, 1997). Scores of less than 9 on the BDI are considered normal and scores of more than 16 are indicative of severe depression. This low mood effect after MDMA has been taken may reflect serotonergic depletion which might be temporary following acute elevation of serotonin induced by MDMA.
Long Term behavioral effects: Gary Van Horn
Surprisingly enough many people who take MDMA have found that after the experience their normal everyday behavior is effected in a positive manner. Many users report being "less materialistic . . . more interested in quality of life," having "increased priority on spiritual matters and relationships," "more focused on education and learning," and a perceived change in their sense of separation from others (Leister et al., 1992). Essentially these users are describing themselves as having had some type of religious experience that seems to have enlightened their spirits and enriched their lives and their behavior, according to their own subjective perceptions of it, has followed suit, making them more talkative, loving, spiritual, and socially functional people, however whether or not MDMA actually has this effect on behavior has not been determined objectively.
Effects Reported by Users: Stephen Richardson
While using the drug ecstasy many people have different sorts of effects. Research shows that there had never been any reports of anyone ever dying from using ecstasy. There have been quite a few cases of overdose usage that was found. The overdose usage had done nothing really but increase the paranoid stage.
Studies show how different people have different types of effects while using ecstasy. Some people's main reason for using the drug is supposed to be for parties called raves. At raves people take the drug so they can go into a pleasure like state of mind. Some people enhance the enjoyment of raves by having the floor lined up with bubble cushions, having a strobe light, and by having a good sound system playing music from the 70's(disco or techtronic music). All of these props add to the effect that one experience while under the influence of ecstasy. The music provides a full bass feeling to the entire body. By this I mean when the bass of a song is real strong deep, your whole body feels like its being rumbled or vibrated each time the bass hits. The srobe light adds an illusionary effect. All the different colored beams of light quickly spin throughout the area, quickly relaxing your mind, and makes you feel like you like your imagining. The lights make it seem like you are in a dreamlike state of mind. Now while you have the bass of the song beating against your body, and you have the lights flashing in a giving you the illusionary effect, you also have the floor padded with this bubble cushion. What this does is gives the feeling as if you are walking on air. From some it is said that if feels like you are literally walking on clouds. Ecstasy makes the body extra sensitive and then you have this air cushion at you feet every time you take a step.
Some people take ecstasy to get the good feeling of being in a dream, or just for pleasure (sex). But what some people don't know is that they are about to find out some things that they may or may not want to have ever known about themselves. For example a woman realized that after taking the drug, that she didn't need to have sex with someone once she first met him to feel pretty. "The reason this experience was so amazing for me was that before knowing these wonderful friends, I had been obsessed with pulling men and sleeping with them, which I now know was to prove to myself and to others that I was attractive…. that night was the first time I had went to the club with friends, and had not thought about sex all night,"(ecstasy.org/experiences, web page). Another experience is a guy who actually kicked his cocaine habit. This guy was addicted to coke for 3 years, and one of his friends told him to try this drug called "X." He did and ended his cocaine habit. "Try this! Its X, its everything you thought Coke would be before you did it…Yes, this is what Coke was supposed to be!"(ecstasy.org/experiences, web page). One woman found out that she really didn't like boys, but was actually a lesbian, and was having sex with guys just so she could feel normal.
I did a personal interview with a friend who I shall call Vanessa who actually took that drug at a rave. She said, "Everything to the touch feels so good…I went around just touching people with my finger and it tingled my whole body. And when I gave someone a hug it felt so good that the hugs lasted for like a minute or two." This enforces that your body feels real sensitive. When I asked her if she would repeat the behavior and go to another one, she replied, "I'm going to my second one in two weeks."
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Chemistry Synaptic Transmitters Effect on Neurons Inhibitory and Exitatory
Ion Channels Effected Physiological Changes Behavioral Changes User Reports