• Lucid Dreaming - Dream Views

    Physiology of Sleep FAQ Updated Feb. 18/05

    Physiology of Sleep FAQ

    This tutorial explains the physiological and biological aspect of sleep. I have assimilated many posts I have made explaining the physiology of sleep in order to create the length annex at the bottom. Because I have assimilated posts of mine fro my past, I may have a few immature or unprofessional comments. I have tried to edit out the irrelevant comments. However, relevant content and points are still assertive (most of the time).

    If you have any questions or suggestions for this tutorial, please feel free to contact me through the most convenient medium to you.

    General topics covered in this tutorial:
    • Sleep patterns
    • stages of sleep
    • biology of sleep
    • sleep facilitation
    • neurotransmitters
    • acetylcholine
    • melatonin
    • serotonin
    • vitamin b6 (pyridoxine)
    • Gamma-Aminobutyric Acid (GABA)
    • drugs & dreams
    • hallucinations
    • sleep paralysis
    • sleepwalking
    • sleep medication
    • temazepam (restoril)
    • triazolam (halcion)
    • zolpidem (ambien)
    • benzodiazepeins
    • blind dreams
    • color & dreams
    • colorblind dreamers
    • nictoine & dreaming
    • tobacco
    • dorsal raphe nuclues (DRN) & dreaming
    • right & left brain functions
    • proprioception during dreaming
    • adenosine
    • caffeine & dreaming
    • marijuana tetrahydrocannabinol (THC)
    • anadamide
    • vertigo

    Sleep Patterns and Stages of Sleep

    During a night of sleep, the brain waves of a young adult record by the electroencephalogram (EEG) gradually slow down and become larger as the individual passes into deeper stages of slow wave sleep. After about an hour, the brain re-emerges through the same series of stages, and there is usually a brief period of REM sleep (on dark area of graph), during which the EEG is similar to wakefulness. The body is completely relaxed, the person is deeply unresponsive and usually is dreaming. The cycle repeats over the course of the night, with more REM sleep, and less time spent in the deeper stages of slow wave sleep as the night progresses.

    Electrophysiological recordings of cerebral activity suggest an approximate neuronal correlate of the milieu (environment) within which conscious experience is unified. The intrinsic electrical activity of the cerebral cortex can change dramatically as a function of the level of arousal and attention. The measurement of electroencephalographic waves obtained by placing electrodes on the scalp, as well as single-neuron recordings in animals, reveal distinct patterns of spontaneous an evoked activity in different states of sleep and wakefulness, including paradoxical or rapid-eye-movement (REM) sleep and attentive states.

    Electroencephalograms of awake and alert subjects display rapid and irregular low-amplitude waves. When the subject closes his eyes and becomes drowsy, the activity becomes regular and rhythmic, with a frequency of about 10 cycles per second. Falling asleep, with loss of consciousness, is accompanied by a gradual transition to much slower waves (1-5 cycles per second) having very large amplitude. From time to time these waves are disrupted by sudden high-frequency burst of low-voltage electrical activity. The slow waves correspond to the phases of REM sleep, which ordinarily are associated with a unique state of consciousness-dreaming. Local high-frequency firings (about 40 cycles per second) are also recorded in alert subjects in attentive states related to the processing of representations in the brain. In recent years there has been a suggestion that these 40 Hz oscillations represent the neuronal correlate of consciousness. Half a century of careful research has shown, however, that much more is involved than this.

    Despite the fact that these electrical activities occur in or near the cerebral cortex, they involve populations of neuron located in nuclei relatively far away from the cerebral cortex, though these neurons are strongly and reciprocally associated with it. The thalamic nuclei play a strategic role in the brain, serving both as generators of internal electrical activity and as relay stations for signals arriving from the external world. Two types of thalamic nuclei are distinguished, corresponding to each of these functions.

    During slow-wave sleep we are not conscious. Often, however, we have a limited, though usually fragmentary, recollection of the dreaming episodes experienced during REM sleep. When we are awake and alert, we are seldom aware that our brains are the seat of intense non-conscious activity. When we are walking or running, for example, we are not usually conscious of the precise position of our feet and joints; nor are we usually aware of the beating of our hearts or the rhythm of our breathing. At any given moment we consult only a small fraction of our repertoire of long-term memories. Whether or not the "unconscious" operates in the manner described by psychoanalysis remains a matter of debate; but its existence is not in doubt, nor that it arises from no conscious operations of the brain that are intertwined with those of our conscious inner life.

    The idea is by no means new. The German philosopher Johann Friedrich Herbart, in Psychologie als Wissenshaft (1824-1825), introduced the notion of a threshold of consciousness beyond which "inhibited" or unconscious ideas become "real" or conscious. About a century later, with the work of Pierre Janet and Sigmund Freud, the question aroused intense speculation, but only recently has it become the object of scientific study.

    Also see: Dream Views' take of the Stages of Sleep

    - Ferdinand Saussure, Cours de linguistique generale (Paris: Payot, 1916, 1995).
    - Neuron, 42(2), M. Dapretto and S. Y. Bookheimer, "From and content: Dissociating syntax and semantic in sentence comprehension," copyright 1999.

    General Synopsis of the Somatic Peripherals of Sleep

    Wakefulness is maintained by activity in two systems of brainstem neurons. Nerve cells that make the neurotransmitter acetylcholine stimulate the thalamus, which activates the cerebral cortex. Full wakefulness also requires cortical activation by other neurons that make monoamine neurotransmitters (MAOI's) such as norepinephrine, serotonin, and histamine. During slow wave sleep, neuron activity in both pathways slows down. During rapid eye movement sleep, the neurons using acetylcholine fire rapidly, producing a dreaming state, but the monoamine cells stop firing altogether.

    The difference is supplied by three sets of nerve cells in the upper part of the brainstem: nerve cells in the locus coeruleus that contain the neurotransmitter norepinephrine; in the dorsal and median raphe groups that contain serotonin; and in the tuberomammillary cell group that contains histamine. These monoamine neurons fire most rapidly during wakefulness, but they slow down during slow wave sleep, and they stop during REM sleep.

    The brainstem cell groups that control arousal are in turn regulated by two groups of nerve cells in the hypothalamus, part of the brain that controls basic body cycles. One groups of nerve cells, in the ventrolateral preoptic nucleus, contain inhibitory neurotransmitters, galanin and gamma-amino butyric acid (GABA). When the ventrolateral preoptic neurons fire, they are thought to turn off the arousal systems, causing sleep. Damage to the ventrolateral nucleus produces irreversible nsomnia.

    A second group of nerve cells in the lateral hypothalamus act as an activation switch. They contain the neurotransmitters orexin and dynorphin, which provide an excitatory signal to the arousal system, particularly to the monoamine neurons. In experiments in which the gene for the neurotransmitter orexin was experimentally removed in mice, the animals became narcoleptic. Similarly, in two dog strains with naturally occurring narcolepsy, an abnormality was discovered for the gene for the type 2 orexin receptor. (I couldn't find out which chromosome or gene, though, sorry). Recent studies show that in humans with narcolepsy, the orexin levels in the brain and spinal fluid are abnormally low. Thus, orexin appears to play a critical role in activating the monoamine system, and preventing abnormal transitions, particularly into REM sleep.

    Two main signals control this circuitry. First, there is homeostasis, or the body's need to seek a natural equilibrium. There is an intrinsic need for a certain amount of sleep each day. The mechanism for accumulating sleep need is not yet clear. Some people think that a chemical called adenosine may accumulate in the brain during prolonged wakefulness, and that may drive sleep homeostasis. Interestingly, the drug caffeine, which is widely used to prevent sleepiness, acts as an adenosine blocker, to prevent its effects.

    What the hell are all these neurotransmitters? O'nus, stop using big words: EXPLAIN!

    Ok ok, sorry. I'll try giving a brief, easy, explanation on some of these neurotransmitters and other commonly discussed neurotransmitters/vitamins (yet again copying a little from older posts I made).

    " class="inlineimg" /> Acetylcholine: The first neurotransmitter to be identified 70 years ago, was acetylcholine (ACh). This chemical is released by neurons connected to voluntary muscles (causing them to contract) and by neurons that control the heartbeat. ACh also serves as a transmitter in many regions of the brain.

    ACh is formed at the axon terminals. When an action potential arrives at the terminal the electrically charged calcium ion rushes in, and ACh is released into the synapse and attaches to ACh receptors. In voluntary muscles, this opens sodium channels and causes the muscle to contract. ACh is then broken down and re-synthesized in the nerve terminal. Antibodies that block the receptor for ACh cause myasthenia gravis, a disease characterized by fatigue and muscle weakness.

    Much less is known about ACh in the brain. Recen discoveries suggest, however, that it may be critical for normal attention, memory, and sleep. Since ACh-releasing neurons die in Alzheimer's patients, finding ways to restore this neurotransmitter is one goal of current research.

    " class="inlineimg" /> Melatonin: Melatonin regulates the physiological changes related by light, the time of day, etc. in co-relation with the suprachiasmatic nucleus. Melatonin pills will immediately inhibit monoamine oxidizers (MAO) which inhibit the production of serotonin which produces melatonin from the pineal gland which is then secreted into the blood stream. Soo, by taking melatonin pills, you kind of skip the process of secretion from the pineal gland and the whole physiological change from serotonin (since melatonin is excreted from serotonin).

    The effects can sometimes take a while depending on the individuals serotonin levels within the digestive tract (there are strong levels of serotonin within the digestive tract to begin with too... alcoholics will be easy to adjust). Since during sleep the levels of melatonin increase dramatically during the waking stage with the arousal of the ascending reticular activation system (A/RAS), by taking melatonin pills, you keep a regular dosage of melatonin throughout sleep without arousal of the ARAS (and waking you up). The amount of acetylcholine is also dramatically reduced during sleep in order to regulate norepinephrine and other neurotransmitters involved with waking state.

    Melatonin can be bought throughout America for, usually, less than $20. It is recommended to take only 2-4mg. (See Proper Intake Times below)

    Melatonin cannot be purchased in Canada... legally

    " class="inlineimg" /> Serotonin: This neurotransmitter, which is released from the pineal gland, is present in many tissues, particularly blood platelets and the lining of the digestive tract and the brain. Serotonin was first thought to be involved in high blood pressure because it is present in blood and induces a very powerful contraction of smooth muscles. In the brain, it has been implicated in sleep, mood, depression and anxiety. Because serotonin controls the different switches affecting various emotional states, scientists believe these switches can be manipulated by analogs, chemicals with molecular structures similar to serotonin. Drugs that alter serotonin's action, such as fluoxetine (Prozac), have relieved symptoms of depression and obsessive-compulsive disorder.

    Serotonin (5-hydroxytryptamine, 5HT) is formed by the hydroxylation and decarboxylation of tryptophan. The greatest concentration of 5HT (90%) is found in the enterochromaffin cells of the gastrointestinal tract. Most of the remainder of the body's 5HT is found in platelets and the CNS. The effects of 5HT are felt most prominently in the cardiovascular system, with additional effects in the respiratory system and the intestines. Vasoconstriction is a classic response to the administration of 5HT.

    Neurons that secrete 5HT are termed serotonergic. Following the release of 5HT, a portion is taken back up by the presynaptic serotonergic neuron in a manner similar to that of the reuptake of norepinephrine. The function of serotonin is exerted upon its interaction with specific receptors. Several serotonin receptors have been cloned and are identified as 5HT1, 5HT2, 5HT3, 5HT4, 5HT5, 5HT6, and 5HT7. Within the 5HT1 group there are subtypes 5HT1A, 5HT1B, 5HT1D, 5HT1E, and 5HT1F. There are three 5HT2 subtypes, 5HT2A, 5HT2B, and 5HT2C as well as two 5HT5 subtypes, 5HT5a and 5HT5B. Most of these receptors are coupled to G-proteins that affect the activities of either adenylate cyclase or phospholipase Cg. The 5HT3 class of receptors are ion channels.

    Some serotonin receptors are presynaptic and others postsynaptic. The 5HT2A receptors mediate platelet aggregation and smooth muscle contraction. The 5HT2C receptors are suspected in control of food intake as mice lacking this gene become obese fromincreased food intake and are also subject to fatal seizures. The 5HT3 receptors are present in the gastrointestinal tract and are related to vomiting. Also present in the gastrointestinal tract are 5HT4 receptors where they function in secretion and peristalsis. The 5HT6 and 5HT7 receptors are distributed throughout the limbic system of the brain and the 5HT6 receptors have high affinity for antidepressant drugs.

    - Lost URL for some sources. If anyone finds it, please let me know.

    " class="inlineimg" /> Vitamin B6: Vitamin B6 is a group of substances pyridoxine, pyridoxal, and pryidoxamine) that are widely distributed in animal and plant tissues. These substances are involved in the metabolism of amino acids (the building blocks of protein) and in the breakdown of glycogen (a stored sugar). Vitamin B6 is found in liver, pork, chicken, fish, and whole grains. A deficiency can result in functional disturbances of the nervous system.

    Pyridoxine is essential in the conversion of amino acids to carbohydrates or fats for storage or energy, the synthesis of new amino acids from carbohydrates, and the conversion of the amino acid tryptophan to niacin. Vitamin B6 provides a role in the development of most protein-related compounds including hormones, neurotransmitters such as serotonin, hemoglobin in red blood cells, and many enzymes.

    The dosage underneath is the Recommended Dietary Allowance (RDA), but be aware that this dosage is the minimum that you require per day, to ward off serious deficiency of this particular nutrient. In the therapeutic use of this nutrient, the dosage is usually increased considerably, but the toxicity level must be kept in mind.

    Males 2 mg per day and females 2 mg per day.

    For those who feel depressed, or any symptoms of depression (lack of self-confidence, loss of will to do anything, loss of desire to wake up, consistently sleeping, etc. etc.) I recommend taking Vitamin B6 or trying to incorporate more food that involve this vitamin before seeking professional help.

    " class="inlineimg" /> Pyridoxine content of Selected Foods, in Milligrams per 3 1/2-oz. (100-gm.) Serving (Murray, 1996)

    (In descending order)
    Yeast, torula - 3.00
    Yeast, brewer's - 2.50
    Sunflower seeds - 1.25
    Wheat germ, toasted - 1.15
    Soybeans, dry - .63
    Walnuts - .73
    Soy bean flour - .63
    Lentils, dry - .60
    Lima beans, dry - .58
    Buckwheat flour - .58
    Blackeye peas, dry - .56
    Navy beans, dry - .56
    Brown rice - .55
    Hazelnuts - .54
    Garbonzos, dry - .54
    Pinto beans, dry - .54
    Bananas - .51
    Avocados - .42
    Whole-wheat flour - .34
    Chestnuts, fresh - .33
    Kale - .30
    Rye Flour - .30
    Spinach - .28
    Turnip greens - .26
    Peppers, sweet - .26
    Potatoes - .25
    Prunes - .24
    Raisins - .24
    Brussels sprouts - .23
    Barley - .22
    Sweet potatoes - .22
    Cauliflower - .21

    - Murray, M. Encyclopedia of Nutritional Supplements. Rocklin, CA: Prima Publishing, 1996.

    " class="inlineimg" /> Gamma-Aminobutyric Acid (GABA): GABA or gamma-aminobutyric acid, discovered in 1950, is the most important and widespread inhibitory neurotransmitter in the brain. Excitation in the brain must be balanced with inhibition. Too much excitation can lead to restlessness, irritability, insomnia, and even seizures. GABA is able to induce relaxation, analgesia, and sleep. Barbiturates and benzodiazepines are known to stimulate GABA receptors, and hence induce relaxation. Several neurological disorders, such as epilepsy, sleep disorders, and Parkinson’s disease are affected by this neurotransmitter.

    GABA is made in the brain from the amino acid glutamate with the aid of vitamin B6. GABA is available as a supplement in vitamin stores, but taking it in pill form is not always an effective way to raise brain levels of this neurotransmitter because GABA cannot easily cross the blood-brain barrier. Companies are searching for ways to place GABA in an oil base in order to ease its entry across this barrier

    GABA can be purchased throughout North America in bottles typically holding 250mg/60 capsules for usually less than $15. It is recommended to only take one 4mg pill of GABA daily.

    Proper Intake of Supplements to Help Induce Lucid Dreams


    It should be noted that these supplements initially, and primarily, only help REMEMBER sleep. These supplements are not "lucid dream pills". By taking one of these pills, you will NOT suddenly have lucid dreams, especially if you have not had one before. Primarily, all these supplements come to the essential production of melatonin, serotonin, and n-methyl-d-aspartate, in order to have the same biological and neurological stasis of the waking state (although complete and parallel balance is impossible). If you believe that these supplements are the reason for your lucidity, then your chances of having lucid dreams without (and even with them) dramatically decrease. To define it to the quintessential point, these supplements only help for these TWO factors:
    - Remembering dreams
    - Prolonging REM sleep

    That's all!

    " class="inlineimg" /> Proper Intake Times: If you have read over the scriptions of these neurotransmitters and supplements, it should be relatively obvious what the order should be, although it depends on your mood (balance of these chemicals in the brain):

    Groggy Bored Mood:
    - Vitamin B6 (60-120min. before retiring)
    - Serotonin (40-60min. before retiring)
    - Melatonin (20-40min. before retiring)

    Excited Anxious Mood:
    - Glass of water, or milk (2-3 hours before retiring)
    - Melatonin (40-60min. before retiring)
    - Serotonin (not recommended, thus, I won't give a time)
    - Vitamin B6 (20-40min, before retiring)

    You can take vitamin b6 once more at the time of going to bed, especially if your diet for the day has been low in this vitamin complex. I, however, do not recommend taking any serotonin supplements. Simply eat the right foods regularly and do not incorporate them into any intake schedules.


    Dreaming occurs during REM sleep, the "paradoxical" sleep stage. Curiously, the ascending acetylcholinergic system actually turns on - it is as though the brain wakes up internally. Yet for some reason the person remains unconscious and unaware. Dreams generally do not make it to conscious memory unless the dreamer is awakened from the dream itself.

    How is it that the cholinergic system can be on and the sleeper still unconscious? The answer probably lies in other neurotransmitters and nuclei of the rostral pons. The dorsal raphe nuclei, a cluster of serotonergic cells, and the locus ceruleus, a group of noradrenergic neurons, also play a role in sleep. They may help to keep consciousness suppressed during dreaming.

    One of the striking things about REM sleep is the absolute stillness of the body. During most stages of sleep we toss and turn, but in REM sleep only the eye muscles twitch (and, for some unknown reason, the middle ear muscles!). This is due largely to a system of descending inhibition. Dreaming turns on a group of cells in the medulla that descend down the spinal cord and inhibit motor activity. Very specific lesions of these cells (a rare event) lead to a phenomenon called "violent sleeping", where the dreamer physically acts out his or her dreams. This is different from sleepwalking, which usually does not occur during REM sleep.


    Another element of the neuronal workspace hypothesis, which has not yet been formalized, has to do with the reportability of conscious experience. The ability to explicitly refer to personal subjective experience is an essential aspect of the definition of consciousness and has particular relevance for the experimental investigation of subjective states, which the subject can describe in one way or another - the simples being to press a button. The possibility of giving such an account depends on the retrieval of memories of past events.

    Hallucinations differ from the conscious recollection of the past in that they spontaneously and involuntarily occur without specific external stimulation. Hallucinations are frequent in schizophrenic patients, and often contribute to the diagnosis of this condition. Hallucinations differ from the conscious voluntary retrieval of long-term memories. Conversely, they exhibit similarities with certain aspects of REM sleep, raising the possibility that hallucinations amount to uncontrolled intrusions of REM sleep into the conscious workspace of the alert subject. Recent brain imaging studies confirm the essential role of the frontal lobe in memory recall. A great many experimental observations had pointed to the involvement of a very old region of the cerebral cortex called the hippocampus. Early imaging studies yielded conflicting results, however, revealing variable and nonreproducible patterns of activation that involved the prefrontal cortex as well as the hippocampal formation. In some cases no activation of the hippocampus was recorded; in others the prefrontal cortex remained silent. Daniel Schachter and his colleagues then realized that the brain images differed depending on whether or not memory retrieval had been successful. From this they concluded that intentional recollection - the effort to search for explicit memories - consistently activates the prefrontal cortex (especially in the right hemisphere), whereas the hippocampus is activated only if conscious recollection has been successful.

    My own personal theory on many hallucinations is maintained around the idea how powerful the subconscious is. Other psychoanalysis’s also believe that hallucinations are simply the mind interpreting what it expects or wants to expect to hear, sound, smell, etc. For example: You could be at work, and there are no customers. You are sitting with your eyes closed and thinking, "Boy it would be nice if a customer came in to give me something to do." Suddenly, you think you hear the door opening and a customer is coming in. You leap up and get ready, but really, it was nothing, or just the sound of you dropping a pen you were holding, a book falling, etc.

    - D. L. Schachter et al., "Memory consciousness and neuroimaging," Phil. Trans. Roy. Soc. Lond. B. 353 (1998): 1861-78.

    Sleep Paralysis & Sleepwalking

    Sleep paralysis occurs when the brain enters slow-wave sleep. The period of slow wave sleep is accompanied by relaxation of the muscles and the eyes. Heart rate, blood pressure and body temperature all fall. If awakened at this time, most people recall only a feeling or image, not an active dream. This also explains the groggy "slow" feeling when awakening. During this time, the afferents responsible for movement are paralyzed in order to keep the body from injuring itself or taking involuntary action during sleep. The somatosensory cortex (the part of the brain primarily responsible for movement and motor control) is essentially, deactivated.

    Quite simply put, sleepwalking occurs when the pathways that are closed off during REM sleep to prevent neurotransmitters from reaching the somatosensory cortex, or any other motor lobes of the brain, open up and allow neurotransmitters to reach these areas, which will then cause the body to act out actions done throughout REM sleep.

    Periodic limb movements of sleep are intermittent jerks of the legs or arms, which occur as the individual enters slow wave sleep, and can cause arousal from sleep. Other people have episodes in which their muscles fail to be paralyzed during REM sleep, and they act out their dreams (sleepwalking). This REM behavior disorder can also be very disruptive to a normal nights' sleep. Both disorders are more common in people with Parkinson's disease, and both can be treated with drugs that treat Parkinson's, or with an anti-epileptic drug called clonanzepam.

    Sleeping Pills

    Often, anti-depressants and anti-anxietals are prescribed to patients suffering from insomnia, although, I will only list the pills specifically designated for sleep.

    Pills Prescribed to Treat Insomnia in order of potency. (Brand names in parenthesis)

    " class="inlineimg" /> Temazepam (Restoril): Like other benzodiazepines (such as diazepam) it enhances the inhibitory action of Gamma-aminobutyric acid (GABA). Metabolized by conjugation with glucuronic acid in the liver, temazepam's peak effect is well absorbed in 2-4 hours after oral administration. Can cause excessive sedation when combined with other CNS depressants. Also, adverse effects include drowsiness, dizziness, headache, fatigue, dependance, and loss of memory. Not to be used by pregnant women.

    Average daily dose: 15mg before retiring.

    " class="inlineimg" /> Triazolam (Halcion): Same as Temazepam; enhances the inhibitory action of GABA. Metabolized in the liver by P-450 enzymes, it's peak effect is achieved within .5-2 hours following oral adminitstration. Triazolam produces additive CNS depressant effects when coadminitstered with other CNS depressants. Should not be taken with other drugs that inihibit CYP3A such as; ketocanozole, itroconazole, and nefazodone. Not to be used by pregnant women.

    Average daily dose: .125 - .25mg before retiring.

    " class="inlineimg" /> Zolpidem (Ambien): Binds to the benzodiaepine receptors and enhances the inhibitory action of GABA. Metabolized in the liver and metabolites are eliminated in the urine after absorption from the Gastro-intestianl (GI) tract. Peak effect in 1-6 hours. Use with caution if using other CNS depressants. Can cause headache, daytime drowsiness, lethargy, and dizziness.

    Average daily dose: 10mg before retiring.

    All other non-prescribed sleeping drugs typically enhance the inhibitory action of GABA, reduces the amount of norepinephrine, dopamine, serotonin, and other incidental excitatory neurotransmitters.

    " class="inlineimg" /> How Do Benzodiazepines Affect Your Body?

    Benzodiazepines are general central nervous system (CNS) depressants. They are all very similar chemically. All benzodiazepines act by enhancing the actions of a natural brain chemical, GABA (gamma-aminobutyric acid). GABA is a neurotransmitter, an agent which transmits messages from one brain cell (neuron) to another. The message that GABA transmits is an inhibitory one: it tells the neurons that it contacts to slow down or stop firing. Since about 40% of the millions of neurons all over the brain respond to GABA, this means that GABA has a general quietening influence on the brain: it is in some ways the body's natural hypnotic and tranquilliser. This natural action of GABA is augmented by benzodiazepines which thus exert an extra (often excessive) inhibitory influence on neurons.

    The way in which GABA sends its inhibitory message is by a clever electronic device. Its reaction with special sites (GABA-receptors) on the outside of the receiving neuron opens a channel, allowing negatively charged particles (chloride ions) to pass to the inside of the neuron. These negative ions "supercharge" the neuron making it less responsive to other neurotransmitters which would normally excite it. Benzodiazepines also react at their own special sites (benzodiazepine receptors), situated actually on the GABA-receptor. Combination of a benzodiazepine at this site acts as a booster to the actions of GABA, allowing more chloride ions to enter the neuron, making it even more resistant to excitation. Various subtypes of benzodiazepine receptors have slightly different actions. One subtype (alpha 1) is responsible for sedative effects, another (alpha 2) for anti-anxiety effects, and both alpha 1 and alpha 2, as well as alpha 5, for anticonvulsant effects. All benzodiazepines combine, to a greater or lesser extent, with all these subtypes and all enhance GABA activity in the brain.

    As a consequence of the enhancement of GABA's inhibitory activity caused by benzodiazepines, the brain's output of excitatory neurotransmitters, including norepinephrine (noradrenaline), serotonin, acetyl choline and dopamine, is reduced. Such excitatory neurotransmitters are necessary for normal alertness, memory, muscle tone and co-ordination, emotional responses, endocrine gland secretions, heart rate and blood pressure control and a host of other functions, all of which may be impaired by benzodiazepines. Other benzodiazepine receptors, not linked to GABA, are present in the kidney, colon, blood cells and adrenal cortex and these may also be affected by some benzodiazepines. These direct and indirect actions are responsible for the well-known adverse effects of dosage with benzodiazepines.

    Contrary to a popular misconception, benzodiazepines do not actually increase the organic synthesis of GABA. As stated, they enhance the action of existing GABA. Actually, benzodiazepines can, over time, decrease the synthesis of GABA in certain areas of the brain. This is one of numerous theories attempting to explain the occurrence of "paradoxical" symptoms
    Benzodiazepine Dependency And Withdrawal FAQ


    Blind Dreams

    I have been doing a little bit of research lately about blind people and dreams and I have turned up quite a bit on my own. So I will now share all the topics of interest in regards to the blind and dreaming.

    Note: If you do not believe in the psychological and neurological aspect on dreaming, or any of the empirical facts of dreaming - Click Here.

    " class="inlineimg" /> What are blind dreams like?

    Helen Keller relating what dreaming was like before her teacher:
    "My dreams have strangely changed during the past twelve years. Before and after my teacher first came to me, they were devoid of sound, of thought or emotion of any kind, except fear, and only came in the form of sensations. I would often dream that I ran into a still, dark room, and that, while I stood there, I felt something fall heavily without any noise, causing the floor to shake up and down violently; and each time I woke up with a jump. As I learned more and more about the objects around me, this strange dream ceased to haunt me; but I was in a high state of excitement and received impressions very easily. It is not strange then that I dreamed at the time of a wolf, which seemed to rush towards me and put his cruel teeth deep into my body! I could not speak (the fact was, I could only spell with my fingers), and I tried to scream; but no sound escaped from my lips. It is very likely that I had heard the story of Red Riding Hood, and was deeply impressed by it. This dream, however, passed away in time, and I began to dream of objects outside myself." (1)
    In studies from the University of California (2) on several patients and their recordings of dreams led to four empirical generalizations:
    1. There are no visual images in the dreams of those born without any ability to experience visual imagery in waking life.
    2. Individuals who become blind before the age of five seldom experience visual imagery in their dreams, although Deutsch (1928) reports some visual imagery in six schoolchildren who lost their sight before age five.
    3. Those who become sightless between the ages of five and seven may or may not retain some visual imagery.
    4. Most people who lost their vision after age seven continue to experience at least some visual imagery, although its frequency and clarity often fade with time.

    What the blind then see's in there dreams is a conglomeration of auditory, gastatory, olfactory, and tactile sensations. One could not exactly portray how the blind interacts with their dreams except by saying, "Close your eyes and walk around the room. That is how the blind dream." The primary reason the majority of people cannot begin to comprehend how blind people can dream is because of the subject perception of dreaming - people who have had sight their whole life have visual dreams nearly 100% of the time, thus it is difficult to imagine dreaming without the visual representation.

    " class="inlineimg" /> Can the blind dream in color?

    First, I must postulate why and how colors are brought into dreaming:

    Colors are typically utilized to amplify images within dreams. Every colors has a certain empathy associated with it and certain objects and scenarios in the world are always associated with a certain color (ie. The Red Cross). Thus, when we see certain depictions within our dreams, our memories will immediately impart the colors into the dream because we believe that they should be there. When the colors are empathetic, it is to portray a certain feeling (ie. Red = anger). Also, colors are implemented into dreams by our memories of the colors, they are not received or projected visually, they are simply memories. The best way to elucidate this is to ask this question, "When you remember things you did years ago, do you usually remember them in color?" The answer, typically, is no - unless the color played a significant role in the memory. This is the same case with dreams, as dreams are the manifestation of thoughts and memories (in the psychological aspect...).

    If the individual had sight before the age of five, it is possible to have the rare experience of seeing a color or even a visual dream. Otherwise, if the blind individual was born blind - they will not even have visual dreams.

    In the research conducted by the University of California, the participants in the study were 15 congenitally and adventitiously blind men and women, ages 24 to 73, with 11 of them between the ages of 44 and 60 (M=46.2; SD=12.5). The ten women and five men in the study were chosen from a larger pool of 16 women and nine men gathered by Hurovitz (1997). They were selected because they contributed at least six recent dream reports that were not labeled as "earlier," "recurrent," or "childhood" dreams over the two-month period they recorded their dreams. In all, they provided 372 dream reports, 236 from the women, 136 from the men.

    Participants whom are congenital blind and totally blind claim that 0% of their dreams were visual, and that 52% of their dreams consisted of taste/ smell/touch (gastatory, olfactory, tactile). There is not even a question whether or not they see color because they do not see at all.

    " class="inlineimg" /> What about the colorblind?

    Also, I should first postulate that the colorblind are this way because of alterations within their retina - their cone photoreceptors, which are responsible for receiving color from the visual hemispheres. For people whom have alterations within their photoreceptors from birth, it is likely that these individuals mix up certain colors for other colors, that we normally see, ie. seeing blue instead of red (please ignore all philosophical debates on whether or not one color is determinate and blah blah blah.. shut up).

    The colorblind are still able to dream in color just as much as any other individual, just their colors will be altered. Of course, if the individual was born without any cone photoreceptors, then they will not dream in color for they have never seen a color. The mind is not capable of spontaneously creating such environments within the dream world becuase dreams work entirely on cognition and recent memories. I have yet to find any experiments on the colorblind, but I will post immediately if I do.

    " class="inlineimg" /> What about the visual cortex of the blind?

    In a study at the deparment of anatomy and neurobiology at the University of Washington, subjects took part in functional magnetic resonance imaging (fMRI) and were required to generate a verb to nouns. In one experiment, blind subjects read the nouns through Braille (Braille task); in a second study, blind and sighted subjects heard the nouns (auditory task). The principal finding from both studies was that blind people had activation foci in visual cortex that corresponded to visually responsive regions noted previously in sighted subjects (3).

    Two-dimensional, flattened views of z-score statistical parameter maps for visual cortex BOLD responses in early and late blind subjects.

    In blind subjects, both tasks evoked extensive bilateral excitation in the lateral visual occipital lobes and Brodmann areas of the brain. This meant that when the blind heard a word, it was not only received through the auditory complex but also precipitated excitatory activity throughout the visutopic areas. The results are significantly more active than those of subjects that had vision.

    What does this mean? I'll elucidate this very easily:
    Your mom screams at you from behind you and you look at her immediately. How you know that she is behind you is the activity of the brain which is drastically increased within the blind as they not only received auditory information, but assimilate a milieu within their mind of their environment. Try picturing what Daredevil see's... only, no vision at all, it is more or less "empathetic". Hopefully that explains it well..

    " class="inlineimg" /> No way, blind people can imagine what vision is like!

    This argument is dialetically arguable.

    Dream about Heliotrophics. You probably can't because it is not real, it is just something I made up while writing this. This is how blind-born individuals perceive vision. Replace heliotrophics with vision.

    Can you please tell me what heaven looks like? (Ignoring the argument of it's existance..) Imagine all you like, you don't know what it actually is - same concept applies to blind people and imagining vision.

    Also take into consideration that the majority of you reading this thread have no clue how it is like for blind people to dream like - invert that thought, because that is the samething that blind people think of you. Can you dream what a blind person dreams? How can you, if you are not blind and never have been?

    Another point (from CT) is imagine what the color tryuipe is like. Don't know what I'm talking about? Can't do it? Exactly.

    Furthermore, the meyer's loop (the information line responsible of relaying information received from the lateral geniculate nucleus (LGN) from the retina, to the occipital lobe) of the blind are nearly, and sometimes completely, inactive. If this loop is not utilised within the youth of the blind individuals life-time, the pathway becomes "lazy" and loses strength as the mind see's (no pun intended) that the loop is not necessary and truly gives no information to cortex. This is the reason why several blind people have a "lazy eye" or their eyes are simply not aligned whatsoever. My point in this is that blind individuals with an inactive visual pathway begin to utilise their visual cortex in association with other senses, primarily auditory. (See 3)


    • 1 - Dreams of the Blind, Richard C. Wilkerson
    • 2 - The Dreams of Blind Men and Women, University of California, Website
    • 3 - Visual Cortex Activity in Early and Late Blind People, Journal of Neuroscience, University of Washington, Website
    • 4 - Malach et al., 1995; Sereno et al., 1995; Tootell et al., 1995, 1996, 1997, 1998; DeYoe et al., 1996; Engel et al., 1997; Hadjikhani et al., 1998



    Nicotine, Dorsal Raphe Nucleus (DRN) & Dreaming

    This asked for some research before I could answer.. and it's still inconclusive. I could not find any correlational research done to determine the direct relationship between nicotine and sleep. However, I did find some articles about the correlation between the dorsal raphe serotogenic activation and dreaming.

    First, yes, there is no serotonin in nicotine. However, it has been shown that nicotine excites dorsal raphe neurons by depolarizing noradrenergic axons, releasing noradrenaline, which then activates alpha1 receptors on serotonin neurons. 1

    In a rat experiment, rats were inject with flesinoxan (a selective 5-HT1A receptor agonist (stimulates serotonin)), and monitored with electorencephalograms (EEG).

    "Male Wistar rats, each weighing 320-350g, were implanted with Nichrome electrodes (200 um diameter) for chronic sleep recordings of electroencephalogram and electromyogram activities by means of placement on frontal and occipital cortex for the former, and on dorsal neck musculature for the latter." 2

    Edit: See the reference link for the graphs which thoroughly explain the experiment. I could link to the graphs and didn't really deem it necessary.

    To sum it up to easily understand, nicotine stimulates vivid dreams. However, they may typically be aggressive dreams. Nightmares may easily precipitate from aggressive dreams simply because of the close biological (and mental) empathetic level. Psychologically, aggressive sleep will produce angry thoughts and frustration. These dreams will cause dreams of profound wish fulfillment usually being the death or murder or an individual. However, with a Jungian perspective, I would say that it would postulate that which in yourself you wish to change and which is flawed - what is causing you the most intrapsychic stress.

    It could be useful.. actually..

    Although, I could not find conclusive correlational research done between nicotine and dreaming, so, it's really just a (logical) hypothesis.

    Tobacco use is the leading prevetable cause of death in the United States. Smokes is responsible for approximately seven percent of total U.S. health care costs, an estimated $80 billion each year (Society for Neuroscience statistic).

    Nicotine acts trhough the weel known cholinergic nicotinic receptor. This drug can act as both a stimulant and a sedative. Immediately aftere xposure to nicotine, there is a "kick" caused in part by the drug's stimulation of the adrenal galnds and resulting discharge of epinephrine. The rush of adrenaline stimulates the body and causes a sudden release of glucose as well as an increase in blood pressure, respiration and heart rate. Nicotine also suppresses insulin output from the pancreas, which means that smokers are always slightly hyperglycemic. In addition, nicotine indrectly causes a release of dopamine in the brain regions that control pleasure and motivation. This is thought to udnerlie the pleasurable sensations experienced by many smokers.

    It is proven that nicotine is, in fact, much more dangerous to the body than marijuana by ten-fold.

    1. Li X, Rainnie DG, McCarley RW, Greene RW (1998) Presynaptic nicotinic receptors facilitate monoaminergic transmission. J Neurosci 18:1904-1912.
    2. Dorsal Raphe Nucleus Administration of 5-HT Receptor Agonist and Antagonists: Effect on Rapid Eye Movement Sleep in the Rat, Jamie M. Monti, Hector Jantos, Daniel Monti and Fernando Alvarino, Department of Pharamacology and Therapeutic Clinis Hospital, Montevideo, Uruguay, 2000 (PDF Format)
    3. "Convergent Excitation of Dorsal Raphe Serotonin Neurons by Multiple Arousal Systems (Orexin/Hypocretin, Histamine and Noradrenaline)", Ritchie E. Brown, Olga A. Sergeeva, Krister S. Eriksson, and Helmut L. Haas, Journal of Neuroscience, October 15, 2002, 22(20):8850-8859


    Right & Left Brain Functions and their Association With Dreaming

    Note: I will make this section more conclusive and thorough in the future. In the meantime, this is a summary from my incidental posts about it.

    To better understand this concept completely, one must understand the functions of the brain. To summarize it:

    Left Hemisphere:
    - Language
    - Logic
    - Interpretation
    - Arithmatic

    Right Hemisphere:
    - Geometry
    - Nonverbal processes
    - Visual pattern recognition
    - Auditory discrimination
    - Spatial skills

    (From The Brain, Pierce J. Howard, Ph.D., Center For Applied Cognitive Studies)

    One most also understand that the brain interacts with it's milieu by utilizing every aspect of the brain. Both hemisphere's are necessary for complete and comprehensive experience. Otherwise, you brink onto alexithymia. Alexithymia dictates that an emotional response is complete if the person is able to (1) to experience emotional feelings (2) to differentiate between various emotional feelings (3) to verbalize his or her emotional feelings (4) to reflect and to some extent analyze these feelings or (5) to fantasize about them. (Reference). Of course this is arguable but logically makes sense.

    The term "Agenesis of the Corpus Callosum" defines when there is a abnormal space or complete absence of hemisphere communication. Because of this miscommunication, individuals with ACC will suffer seizures and essential ataxia (loss of the ability to coordinate muscle movement). This causes problems with walking, eating, breathing, articulating, etc. Also, there may be impaired visual and auditory memory (or lack thereof). Worst of all, it is very possible for hydrocephaly to occurr. Hydrocephaly is the abnormal collection of fluid within the missing spaces that may destroy much neural tissue and caues mental disorders. Since ACC is most commonly congenital, there is a great possibility for retardation.

    It is these factors that argue alexithymia - do dreams matter if you cannot comprehend them or even remember them? Can significant dreaming occurr in individuals with ACC? "If a tree falls in a forest and no one is around to hear it, does it make a sound?" Keeping in mind that if someone with ACC was nearby they would most likely commit to seizure before anything else.

    My point in all of this was to state that the hemisphere's are both equally responsible for dreaming and brain processing. A point that Howetzer made postualtes this further:

    Both hemisphere's are responsible for every process. Yes, there are certain aspects of the brain that are the neurological initial stage of sensory reception; but if this were the deciding factor on what is the most important and conscious part of the brain, then your answer would simply be the thalamus. If not, then the hippocampus or simply memory.

    Also, all organisms have a concept of language and auditory sounds - it's the recognition and association to meaning that is recieved within the human brain. This is merely memory. Consider that other animals still recognize loud and scary sounds, tones (how a dog acknowledges you, etc.), and even some animals have much more advanced hearing and recognition than humans (cats, for example).


    Proprioception & Dreaming

    When we sleep, we were essentially cut off from the sensory world. There is no auditory, gastatory, olfactory, or feeling sensations. We would not even see if our eyes were peeled open.

    This is because when you are asleep, the following happens (or doesn't happen):
    - Acetylcholine (ACh) system becomes inactive
    - Sensory thalamus inhibited
    - Reticular nucleus active
    - Thalamocortical neurons in slow rhythm
    - EEG synchornous

    Also, during sleep the dorsal raphe nuclei (a cluster of serotonergic cells) and the locus ceruleus (a group of noradrenergic neurons) help to keep consciousness suppressed during dreaming. During REM sleep, only the eyes muscles twitch (hence Rapid Eye Movement) but the middle ear muscles also twitch, for an unknwon reason. This occurrs mostly because of the descending inhibition. Dreaming turns on a group of cells in the medulla that descend down the spinal cord and inhibit motor activity. Very specific lesions of these cells (a rare event) lead to a phenomenon called "violent sleeping", where the dream physically acts out his or her dreams. This is different from sleepwalking, as sleepwalking does not occur during REM sleep.

    If there is any possibility of auditory perception during sleep, it would be because the auditory nerve carries it's signals all the way to the brainstem which synapses with the cochlear nucleus. From here, the auditory sense eventually reaches the medial geniculate nucleus and then into the auditory cortex. If this occurs, it is very incidental and very rare.

    What to keep in mind is that, during slow wave sleep, neuron activity significantly slows down. Neurotransmittesr such as norephinephrine, serotonin, and histamine are at very low reproductive states. However, during REM, ACh fire rapidly, producing a dreaming state, but the monoamine cells stop firing altogether. Do not confuse this with what I said above; ACh does not fire during the first few stages of sleep, but only in REM period.

    Proprioception occur's within the cerebellum, which is facilitates by monoamine cells. Since there is no production of monoamine cells within the period of dreaming, propriocetion is impossible. If there is any sense that you feel your body or are "aware" of it, it is most likely your memory recalling the sense. Primarily, your memory facilitates all that occur's within your dreaming states and your sensory perception - hence why you dream in a visual state.


    Caffeine & Dreaming

    As I stated above in this tutorial, there are two main signals that control the cicruitry of sleep. First, there is homeostasis, or the body's need to seek a natural equilibrium. There is an intrinsic need for a certain amount of sleep each day. The mechanism for accumulating sleep need is not yet clear. Some people think this chemical called adenosine may accumulate in the brain during prolonged wakefulness, and that i may drive sleep homeostasis. Caffeine acts as an adenosine blocker.

    The effects of caffeine on human information processing have been well reviewed.* A large number of studies has been performed on human subjects (Estler, 1976; Daly et al., 1993). As for most effects of caffeine, the dose-response curve is U-shapeddoses of 500 mg causing a decrease in performance although lower doses have positive effects (Kaplan et al., 1997). Despite this, increases in caffeine consumption over an already high normal level (400-1000 mg/day) did not impair performance even in a complex setting (Streufert et al., 1997). Revelle and coworkers (1980) showed a complex interaction between the effects of caffeine on performance and parameters such as personality and time of day. Thus, the effects of caffeine are related to a level of arousal (Anderson and Revelle, 1982) and largely follow the so-called Yerkes-Dodson law that postulates that the relationship between arousal and performance follows an inverted U-shape curve. An increase in arousal improves performance of tasks where relatively few sources of information have to be monitored, particularly under conditions when the need for selective attention is stressed by time pressure. When, on the other hand, multiple sources of information or working memory have to be used, an increase in arousal and attention selectivity has no apparent beneficial effect on performance, which may consequently even decrease (see Kenemans and Lorist, 1995). Thus, it was concluded that caffeine increases cortical activation, increases the rate at which information about the stimulus accumulates, increases selectivity particularly with regard to further processing of the primary attribute, and speeds up motor processes via central and/or peripheral mechanisms (Kenemans and Lorist, 1995). In a study where caffeine significantly improved performance in a vigilance test, caffeine neither increased nor decreased the mood changes that occur after such stressful tasks (Temple et al., 1997).

    Therefore it can probably be concluded that caffeine in doses that correspond to a few cups of coffee "improves behavioral routine and speed rather than cognitive functions" (Battig et al., 1984). This probably indicates that many animal models test for psychomotor function rather than cognition, but it is of course very different from claiming that "caffeine bestows little if any benefit on... psychomotor performance" (James, 1991). The small benefits that can be shown may be considered of value by some caffeine users, and it can be expected from the above considerations that, particularly, individuals with a low level of arousal (high scores on the impulsivity subscale of Eysenck) should experience such a beneficial effect. Indeed, such individuals appear to consume more caffeine (Rogers et al., 1995). Conversely, in situations with a high level of stress, caffeine might prove detrimental, but there is no evidence that this is the case (Smith et al., 1997).

    In order to perform adequately, an animal (or human) must be able to filter out irrelevant sensory input. A deficiency in this regard is believed to be a characteristic of schizophrenic subjects (Koch and Hauber, 1998). Filtering ability can be assessed by so called prepulse inhibition of the acoustic startle response (see Hauber and Koch, 1997; Koch and Hauber, 1998). Such prepulse inhibition can be attenuated by systemic or intra-accumbens administration of apomorphine, and this is counteracted by an injection of the adenosine A2A agonist CGS 21680 into the nucleus accumbens (Hauber and Koch, 1997). These results suggest that caffeine might, via an action on adenosine receptors, influence sensorimotor gating and, in this way, performance.

    * van der Stelt and Snel, 1993

    Marijuana, Tetrahydrocannabinol (THC) & Dreaming

    Marijuana can distort perception, and alter the sense of time, space, and self. In certain situations, marijuana can produce intense anxiety. In radioactive tracing studies, scientists at the Society for Neuroscience and the University of Washinton found that tetrahydrocannabinol (THC), the active ingredient in marijuana, binds to specific receptors, many of which coordinate movment. This may explain why people who drive after they smoke marijuana are impaired. The hippocampus, a structure involved with memory storage and learning, also contains many THC receptors. This may explain why heavy users or those intoxicated on marijuana have poor short-term meory and problems processing complex information ("Dude... what did you just say?" "I don't know man..." "I'm so high"). Scientists recently discovered that these receptors normally bind to a natural internal chemical called anandamide, and are now working to see how this natural marijuana affects brain function.

    The properites of tetrahydrocannabinol (THC) do not effect the production of acetylcholine or, at least, dramatically effect the process of falling asleep. The most active receptors of THC are within the hippocampus which is where memory is stored. Activity within the hippocampus with THC will produced sporadic dreaming, but would most likely not help with much else other than that. So, you'll dream as though you're projecting your sporadic, short attention spanned, thoughts.

    Generally, the results are that the content of dreams affected by THC are very sporadic and tend to have no cohesion whatsoever. Due to the abundant THC receptors within the hippocampus integrated with the various other residual neruological effects of THC (pineal, primarily), the dreams of THC effected dreams are generally sporadic, if recalled at all.

    Apparently THC also has effects on the internal chemical called anadamide, but I have yet to find much more information on that besides the reference below.

    Reversal of Dopamine D2 Receptor Responses by an Anandamide Transport Inhibitor, Massimiliano Beltramo1, Fernando Rodreguez de Fonseca2, Miguel Navarro2, Antonio Calignano4, Miguel Angel Gorriti2, Gerasimos Grammatikopoulos5, Adolfo G. Sadile5, Andrea Giuffrida3, and Daniele Piomelli1, The Journal of Neuroscience, May 1, 2000, 20(9):3401-3407


    Vertigo & Dreams

    Vertigo occurs because a part of your body has sent a confusing message to your brain.

    To better understand why this may occur, one must first understand what makes us feel balanced - how the brain perceives that we are standing upright. This is facilitated by the vestibular system. Doctors may tell you that your inner ear is to blame for the vertigo sensation because this is where the vestibular system is located.

    The vesitbular systems functions with a system of hair-like calcium carbonate. These are found within the otolithic organ. These hairs stimulate the membrane they rest on by gravity. Further into the ear, there are semicircular canals. These canals are filled with the liquid endolymph. When we move our body, the endolymph moves, when the endolymph moves out-of-control and creates inertia. Thus, even though you are not moving, the endolymph has enough inertia to continue moving and signal to your brain that your are moving. Other signals contradict and confuse one another to create the feeling of vertigo.

    This adds to the theory that dreams are somatically induced. Many individuals who have ear infections will complain about dreams about vertigo or falling. When I was young, I had a severe ear infection myself. I found that I had many dreams of falling and intense vertigo. Also, keep in mind that during REM sleep, middle ear muslces are stimulated (for unknown reasons). This may also have an influence on the vertigo feeling you are experiencing.



    I am not a certified physician nor a pharmacologist. I am a psychology student. This information is all collected from my scholarly studies.

    The information in this section is intended only to assist the reader utilizing this website. It is not necessarily a definitive statement on the subject. The authors hereby disclaim any responsibility for liability, including but not limited to liability for negligence, which might arise due to any acts or omissions, directly, or indirectly, on the part of the person utilizing this website. A person\'s needs must be assessed on an individual basis, often in consultation with a qualified healthcare professional, utilizing procedures appropriate to that individual\'s needs.

    Thank you for reading my tutorial. I hope I have been enlightening.
    ~ Michael † O\'nus

    Created by , 07-02-2004 at 04:52 AM
    Last edited by , 09-21-2010 at 10:56 PM
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