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Courtney Neff

on 19 February 2013

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Transcript of LSD

LSD Group 1 Adam D'Ovidio, Aditya Thiyagarjan, Alexander Field, Alicia Yu, Courtney Neff, Harveer Dhupar, Kimberly Luoma LSD, or lysergic acid dimethylamide is a psychotomimetic drug found in 1938. LSD acts in the brain, and is an agonist of the 5-HT1A and 5-HT2A receptors, while possibly having both agonistic and antagonistic effects on the D1 and D2 receptors. It is most well-known for its psychedelic effects after administration. LSD has been known to assist in treatment of those suffering from depression or alcohol addiction in the past. The most common route of administration is orally or sublingually. LSD is absorbed in the gastrointestinal tract, is distributed all over the body, is metabolized in the liver, and is eliminated via urine. A lethal dose of LSD would range anywhere from 200 µg/kg to over 1mg/kg of body mass, or 12,000 µg in general. Side effects of taking LSD include hallucinations, synesthesia, and vasoconstriction. LSD should not be taken if one is pregnant, has hypertension, or taking any other hallucinogenic, antipsychotic, or antidepressant drugs. Abstract Lysergic Acid Diethylamide (LSD) is an extremely powerful hallucinogen that was first developed in 1938 by Albert Hoffman. Its abbreviation comes from the original German name Lyserg-Saure-Diathylamid. LSD is considered to be one of the most potent drugs of its kind, distorting the user’s perception of reality, emotional state, sensory system and brain function. It is used recreationally for both the hallucinations and “high” that it creates. LSD is also used as an entheogen, a drug that is taken for the purposes of inducing a spiritual or mystical experience. LSD was first synthesized from lysergic acid, which can be found in a fungus called ergot that grows on rye grass, and is now synthetically manufactured in illegal labs. The effects of LSD are unpredictable and dangerous, and the drug has been determined to have no legitimate use as a medical treatment. Thus, the drug was prohibited in 1971 under the United Nations Convention on Psychotropic Drugs, making it illegal in many countries including Canada, the United States, and much of Europe. Today in Canada the possession of LSD can carry a maximum penalty of a 6 months’ imprisonment or a $1000 fine for a first time offense. Introduction IUPAC Name: (6aR, 9R)- N,N- diethyl- 7-methyl- 4,6,6a,7,8,9- hexahydroindolo- [4,3-fg] quinoline- 9-carboxamide

Generic Name: Lysergic acid Diethylamide, or Lysergsäure-diethylamid in German

Other Names:
• N,N-diethyl-lysergamide, and LSD-25
• The International Non-proprietary Naname is (+)-lysergide
• Colloquial Names
o LSD Alone
 Acid, Yellow Sunshine’s, Battery Acid, Blotter, Dots, Electric Kool-Aid, Window Pane, Purple Haze, Sugar Cubes, Elvis, Blue Cheer
o LSD Combinations
 Candy-flipping – LSD and MDMA
 Frisco Special – LSD, cocaine, and heroin
 Outer Limits – Crack and LSD
 Black Acid – LSD and PCP
o LSD Users
 Acid freak/head, Explorer’s Club (group of LSD users)
o Other Slang
 Yen Sleep - restless, drowsy state after LSD use

Molecular Formula: C20H25N3O

Molecular Weight: 323.43 g/mol Other Names Figure 2. Molecular structure of LSD Figure 1. Albert Hoffman; the Swiss chemist who discovered LSD The mechanism of action of LSD is not a well understood topic. This is because of the number of receptors that it can interact with. LSD acts to preferentially inhibit serotonergic cell firing while sparing postsynaptic serotonergic receptors from up regulation/down regulation. The action of 5 HT is key in understanding the function of LSD. 5-HT is produced by a small number of neurons most of which lie in the raphe nuclei (RN) of the midbrain. One major target of the RN is the locus coeruleus (LC), which controls the release of norepinephrine, which regulates the control of the sympathetic nervous system.

LSD acts on multiple receptors as:
• An agonist on the 5-HT1A receptor in the LC, the RN and the cortex. The 5-HT1A receptor is an inhibitory receptor. Thus the binding of LSD results in inhibition of firing and serotonin release. Studies have shown that at moderate to higher levels LSD may actually activate postsynaptic serotonin receptors in place of serotonin.
• An agonist on the 5-HT2 receptor. Most data shows that it is a specific 5-HT2A but a 5-HT¬2C cannot be ruled out. Activation of this receptor leads to increased levels of cortical glutamate levels. Glutamate is the most abundant excitatory neurotransmitter in the vertebrate nervous system. This may explain part of the hallucinogenic effects of LSD.
• There is also evidence of LSD interacting with the dopaminergic system; it interacts agonistically and antagonistically with D1 and D2 receptors. This mechanism is not well understood. Mechanism Of Action It acts as an agonist of the 5-HT1A receptor. The mechanism of this activation is as follows:
•The LSD first binds to the 5-HT1A which is a G protein coupled receptor (GPCR). This GPCR is associated with the Gi subunit.
•Once the receptor is activated, the G subunit is activated and it binds to adenyl cyclase and deactivates it.
•This decreases the amount of cAMP being produced and thus inhibits cell functions mediated by cAMP.
•At moderate to higher levels though LSD may act as a postsynaptic serotonin receptor agonist

It acts as an agonist of the 5-HT2A receptor. The mechanism of this activation is as follows:
•The LSD first binds to the 5-HT2A which is a G protein coupled receptor (GPCR). This GPCR is associated with the Gq subunit.
•Once the receptor is activated the G subunit dissociates from the receptor and activates the Phospholipase C (PLC) which in turn hydrolyzes phosphatidylinositol (PI2) to diacyl glycerol (DAG) and inositol triphosphate (IP3). IP3 then acts as a second messenger that activates protein kinase C (PKC) it also binds to IP¬3 receptors particularly calcium channels in the endoplasmic reticulum (ER).

The activation of different receptors in the serotonergic system then leads to the psychedelic effects of LSD. It is also to be noted that receptor activation by LSD is time dependent. Where 15 to 30 min after administration the main class of receptors being affected are the 5-HT receptors and after about 90 minutes the D2 receptors play a bigger role. Clinical Indications
One should not take LSD:
•If taking any antipsychotic or antidepressant drugs
•If taking any other hallucinogenic drugs, as it may lead to an overwhelming state of mind
•If suffering from a mental illness, as effects of LSD may exacerbate existing disorder
•If suffering from hypertension
•If previous history of tachycardia or cardiac abnormalities
•If pregnant, as LSD can cause uterine contractions and could negatively impact a pregnancy
•In combination with chemotherapeutic drugs
•Because it is illegal!! Contraindications Unwanted Effects Major:
•Long-lasting psychoses (depression and schizophrenia)
•Irreversible brain damage (constant “tripping”)
•Impaired short-term memory

•Reduced/increased appetite
•Increased heart rate and body temperature
• Acid “flashbacks”, in which parts of an acid experience are re-lived after the drug has worn off
•Hallucinations/Altered perceptions of time and reality
•Psycho-physical dissociation Administration: Blotter LSD can be swallowed or taken sublingually. Liquid LSD is commonly dropped straight onto the tongue or in the eye. LSD can also be inhaled and injected intravenously. The absorption occurs rapidly in the gastrointestinal tract.

Distribution: LSD diffuses into all tissues of the body and crosses the blood-brain barrier.

Metabolism: The effects of LSD take place gradually within 30-60 minutes after taking the drug, and reach peak within 2 to 4 hours and diminish within 10-12 hours.
LSD is metabolized in the liver.

Excretion: LSD has an elimination half life of 175 minutes and is excreted through urine. Pharmacokinetics
A standard dose with noticeable hallucinogenic effects is about 20-80μg. Threshold effects can be felt with as little as 20μg. Experienced users typically administer 100-200μg for a “good high”. A single LSD blotter usually contains between 30 - 100μg of LSD. A single drop of potent liquid LSD could be 50 times a normal dose. The dosage of a single square of gelatin LSD (mixing liquid LSD with gelatin and forming it into small squares) ranges between 50 and 150μg. Dosage LSD Oral Dosage
Threshold: 20µg
Light: 25-75µg
Common: 50-150µg
Strong: 150-400µg
Heavy: >400µg
Lethal Dose: >12,000µg Toxicity •It is estimated that the LD50 for LSD is in a range from 200 µg/kg to over 1mg/kg of body mass, or in general, any dose over 12,000µg
•Reports have shown that cases regarding overdose are minimal to none
•Some sources report an overdose in Kentucky in 1975 where a man was injected, via IV, with about 320mg. This is an extremely large amount of LSD to take through IV (case still controversial)
•Due to lack of recorded overdoses, sources vary regarding the estimated lethal doses for humans. Alternative Drugs Fun Facts! • Albert Hoffman also ingested the first intentional dose of LSD of 250 µg, this was on April 19, 1943. To study the effects that he discovered after the first accidental dose.
• To be in possession of LSD was finally made illegal in the United Sates on October 24, 1968
• LSD comes in a variety of colors and shape the evolution of how LSD came to look the way it does today is as follows:
o Was first sold in what looked like sugar cubes
o Was then changed into a tablet form
o In 1968 LSD appeared in a bright orange tablet (measured roughly 6mm across) was given the nick name “Orange Sunshine” – acid was the first form of LSD that became widely available after it was made illegal to be in possession of the drug
o Then came “computer acid” or “blotter paper LSD.” This is generally what we think of when LSD comes to mind, many colors and a variety of different designs can be made
o Since 1969 over 200 types of LSD tablets have been notes
o Since 1975 over 350 blotter papers have been notes
•In the 1950s the US Central Intelligence Agency administered LSD to CIA employees, military personnel, doctors, other government agents, mentally ill patients, and members of the general public under a research program in order to study their reactions to the drug without the persons knowledge that they had ingested the drug – the code name of this operation was Project MKULTRA
•The Beatles hit song, “Lucy in the Sky with Diamonds”, is said to be about LSD by Paul McCartney himself. Figure 8. Blotter paper LSD – one among many blotter paper images Figure 3. a) A close up of the 5-HT1A receptor as is found in the post-synaptic membrane of a neuron, b) The specific mechanism of action of the 5-HT1A receptor a) b) Figure 4. The activation of glutamate by stimulated 5-HT1A and 5-HT2A receptors Figure 5. An overview of the diversity of LSD receptors The effects of LSD normally depend on dosage, tolerance, body weight, age, and sex. It is a potent psychotomimetic drug that causes sensory distortion and hallucination. However, there is no significant clinical value of its use and it is not an approved drug. Some of its potential uses are:

An recreational drug as a hallucinogen
An entheogen for spiritual purposes
An agent in psychedelic therapy (therapeutic practices involving the use of psychoactive drugs):
o Treats alcoholism
o Relieves anxiety in terminal ill patients

Treats some forms of schizophrenia
Reduces cluster headache ( an immense degree of pain on only one side of the head)
An analgesic for serious and chronic pain caused by cancer or other major trauma
Other uses in psychotherapy:
o Personality disorder
Transient situational personality disorder
o Psychoneurotic disorder (mental disorder that causes deficit in functioning) Works Cited There are many drugs that produce a similar effect to LSD. LSB, a designer drug developed in the fifties, is an isomer of LSD. A single butyl group joined at the second carbon has replaced the two ethyl groups of the amide nitrogen. Studies in rats have revealed that while LSB is a more potent 5-HT1A agonist than LSD, it is a weaker 5-HT2A agonist. Therefore it produces a weaker effect in humans than LSD.
Like LSB, LSZ is another synthetic LSD analogue with the diethylamide group constrained into an azetidine ring, creating 3 stereoisomers around this ring. An alternative 5-HT2A agonist is dimethyltryptamine, or DMT. DMT is found in many plants and is produced in small amounts in mammals. In humans it functions as an amine neurotransmitter and modulator. DMT affects most of the serotonin receptors, but has been shown to be an agonist of the 5-HT1A, 5-HT2A, and 5-HT2c receptors. Like LSD, DMT produces powerful psychedelic and visual effects including short periods of euphoria and hallucination.
DPT (dipropyltryptamine) is a synthetic DMT analogue that shares a very similar chemical structure to DMT, but has been reported to have very different psychoactive effects. Some experiences include a loss of boundaries, experiencing someone else’s life for them, and experiencing the universe from different positions in time and space. DPT is also used by a religious organization known as the Temple of True Inner Light, where it is believed that DPT is a physical manifestation of God. The best part is that LSB, LSZ, and DPT are designer drugs so they are commercially available for purchase, unlike LSD. Figure 6. Structure of LSB Figure 7. The structural comparison between DMT and DPT Abbas A.I.,et al. (November 2009). "Predicting new molecular
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