Textbook Chapter 15. Psychedelics

Tolerance to LSD develops quickly within 1-3 days of repeated use, leading to near-complete loss of its effects.

The mechanism behind LSD tolerance is the downregulation of serotonin 5-HT2A receptors, which are crucial for its effects.

LSD tolerance disappears relatively quickly, and sensitivity to the drug returns within a week.

Cross-tolerance occurs between LSD, psilocybin, and mescaline, meaning tolerance to one leads to tolerance to the others.

DMT is an exception to the rule, as tolerance does not build up with repeated use, unlike other classic hallucinogens.

No withdrawal symptoms have been documented for LSD or similar drugs.

Hallucination persisting perception disorder (HPPD) is a rare perceptual disorder that can occur after using hallucinogens.

Classic hallucinogens like DMT, mescaline, and psilocybin are often used in spiritual or ceremonial contexts.

The locus coeruleus (LC) plays a key role in novelty detection and fear responses. It receives input from sensory sources and sends projections to various brain regions, including the cortex, where it promotes the release of norepinephrine (NE).

Classic hallucinogens like LSD and mescaline suppress the activity of the locus coeruleus (LC) by acting on 5-HT2A receptors. This suppression, along with enhanced LC response to novelty, contributes to the perception-altering effects of these drugs.

Hallucinogens, particularly LSD, act as agonists at 5-HT1A receptors in the raphe nuclei, inhibiting neuronal firing and serotonin release. This suppression of the raphe system can subsequently lead to suppression of the LC.

LSD acts as an agonist at 5-HT2A receptors in the cortex, increasing the duration of excitatory action potentials in glutamatergic neurons. This effect is most prominent in the medial prefrontal cortex, which is involved in information processing and perception.

The effects of LSD on the body, like pupil dilation, nausea, and increased heart rate, depend on the dosage taken. While these effects are often present, they are rarely life-threatening.

The tendency for the effects of a drug to lessen with repeated use.

A state of heightened anxiety, fear, and panic experienced during a hallucinogenic trip. It's often triggered by losing sight of the drug-induced nature of perceptions.

A drug-induced perceptual alteration that may reappear days, months, or years after ingesting a hallucinogen, often accompanied by anxiety.

A condition characterized by persistent perceptual disturbances, such as visual distortions, occurring days, months, or years after hallucinogen use.

Classic hallucinogens, like LSD and psilocybin, are unlikely to cause damage to vital organs like the heart, liver, or kidneys.

Classic hallucinogens are unlikely to cause a fatal overdose.

Certain designer hallucinogens, such as 5-MeO-DIPT, 5-MeO-DALT, and AMT, have higher risks associated with them.

The experience of hallucinogenic drugs is heavily influenced by the individual's psychological state and the environment.

Panic reactions during a bad trip are often caused by high doses or mixtures of drugs, but are usually manageable with reassurance and calm.

Individuals with mental health vulnerabilities may experience prolonged psychotic or depressive symptoms after using hallucinogens.

The ability of LSD to evoke emotional breakthroughs and insights into one's inner self, often revealing repressed thoughts and emotions.

A term coined by Humphry Osmond to describe the ability of hallucinogens to help people connect with their inner emotions and thoughts.

A state of heightened awareness and sensory perception often experienced under the influence of LSD, where colors appear brighter, sounds seem sharper, and the senses are amplified.

A term that describes the perceived effects of LSD in relation to sensory perception, often resulting in heightened awareness of sights, sounds, and other stimuli.

A comparison between the insights gained from LSD experiences and those achieved through psychoanalysis, both revealing deeply buried emotions and thoughts.

The potential therapeutic use of LSD in psychotherapy, proposed by Humphry Osmond, based on its ability to facilitate emotional breakthroughs and uncover hidden feelings.

The subjective experiences reported by individuals under the influence of hallucinogens, including altered perception, emotional insights, and often profound philosophical or spiritual realizations.

A heightened awareness of the self and the interconnectedness of all things, often experienced under the influence of LSD, where one may feel a sense of unity with the universe or with other beings.

The subjective experiences reported by Bernard Aaronson after taking LSD in an experiment, showcasing emotional release, introspection, and insights into personal relationships.

LSD is absorbed through the digestive system and reaches the brain 1% of the time. It has a half-life of 175-300 minutes, with effects lasting 10-12 hours.

A type of psychedelic drug that causes visual and auditory hallucinations.

LSD, psilocybin, and DMT are indolamine hallucinogens that are highly selective in their binding and primarily target 5-HT2A receptors.

LSD, unlike other serotonin receptor agonists, trigger distinct intracellular signaling cascades within cortical neurons.

Mescaline is another classic hallucinogen extracted from cactus flowers.

Mescaline is quickly absorbed from the digestive system and has a similar half-life as LSD.

LSD and other hallucinogens may affect dopamine and adrenaline receptors.

LSD and other classical hallucinogens, though studied for many years, still have aspects of their effects on the Central Nervous System (CNS) that are not fully understood.

LSD is considered an agonist at serotonin receptors in the brain, activating these receptors.

LSD behaves as an antagonist at serotonin receptors in the peripheral nervous system, blocking their activity.

The use of classic hallucinogens does not usually escalate over time, unlike substances like alcohol or nicotine.

Classic hallucinogens are unlikely to cause damage to vital organs like the heart, liver, or kidneys.

A condition characterized by persistent perceptual disturbances, such as visual distortions, occurring days, months, or years after hallucinogen use.

LSD, psilocybin, and DMT are examples of hallucinogens that are highly selective in their binding to serotonin receptors. They primarily target 5-HT2A receptors, but also influence other subtypes like 5-HT2B and 5-HT2c.

LSD and other hallucinogens, despite their long history of use, still present some mysteries in how they affect the central nervous system. More research is needed to fully understand their intricate mechanisms.

Classic hallucinogens, like LSD and psilocybin, typically don't cause life-threatening harm to vital organs like the heart, liver, or kidneys.

Classic hallucinogens have a low risk of causing a fatal overdose.

Certain designer hallucinogens, such as 5-MeO-DIPT, 5-MeO-DALT, and AMT, have higher risks associated with their use.

The experience of hallucinogenic drugs is greatly influenced by the individual's emotional state and the surrounding environment.

Panic reactions during a bad hallucinogenic trip are often caused by high doses or drug mixtures, but can usually be calmed down with reassurance and a calm voice.

Individuals with pre-existing mental health vulnerabilities may experience extended psychotic or depressive symptoms after using hallucinogens.

Hallucinogen Persisting Perception Disorder (HPPD) is a condition characterized by persistent perceptual disturbances, like visual distortions, that can occur days, months, or even years after using hallucinogens.

Flashbacks are a type of perceptual alteration that may reoccur days, months, or years after taking a hallucinogen, often accompanied by anxiety.

Tolerance to LSD develops rapidly within 1-3 days of repeated use, leading to a near-complete loss of its effects.

Tolerance to LSD disappears relatively quickly, and sensitivity to the drug returns within a week.

Salvinorin A primarily acts on the kappa-opioid receptor system, a different pathway than classic hallucinogens like LSD.

Salvinorin A produces effects like antinociception, hyperthermia, sedation, and reduced motor activity in rodents.

While Salvinorin A is potent, it shows low toxicity. Even high doses don't cause evident damage to vital organs in mice.

Salvinorin A produces a rapid onset of perceptual and mood changes. Some users experience positive effects, while others feel anxiety or disorientation.

Salvinorin A can cause altered states of consciousness, changes in perception of reality, and altered sense of time.

Salvinorin A can lead to loss of control, panic attacks, racing thoughts, and social withdrawal.

Salvinorin A can distort bodily perception, merge objects with surroundings, and create intense visual experiences.

Salvinorin A's effects, while intense, fade quickly, and it doesn't cause long-lasting physical harm.

Salvinorin A's effects are primarily attributed to its interaction with kappa-opioid receptors, a distinct pathway from classic hallucinogens like LSD.

Salvinorin A's diverse effects, both positive and negative, emphasize the importance of understanding individual user experiences and the potential dangers of this potent substance.

Salvinorin A is a psychoactive compound found in Salvia divinorum, a plant in the mint family known as "diviner's sage." It's stored in glandular trichomes, similar to how cannabinoids are stored in Cannabis.

The Mazatecs, indigenous people of Oaxaca, Mexico, have used Salvia divinorum for centuries in healing and divination ceremonies. They call it the "leaf of prophecy" due to its ability to induce visions.

Salvinorin A, unlike other hallucinogens, is a diterpene, making it chemically distinct from alkaloids like LSD or mescaline.

Salvinorin A has hallucinogenic and dissociative effects, similar to cannabis, ketamine, and high doses of classic hallucinogens. However, it's considered particularly intense by experienced hallucinogen users.

The Mazatecs traditionally use Salvia divinorum orally by chewing fresh leaves or blending them with water. Modern recreational users typically smoke the leaves, using a pipe, bong, or vaporizer.

Salvinorin A is a highly selective kappa (κ)-opioid receptor agonist. This means it specifically activates κ-opioid receptors in the brain.

Salvinorin A is a potent hallucinogen, with as little as 200 micrograms producing noticeable effects. This makes it comparable in potency to synthetic drugs like LSD.

Salvinorin A has a short duration of action, typically lasting about 60 minutes. The effects start within 5-10 minutes after smoking and build up gradually.

Salvinorin A is absorbed primarily through the lungs when smoked. It's not effectively absorbed sublingually or orally.

Salvinorin A's effects are largely attributed to its activation of κ-opioid receptors in the brain. This leads to the unique and intense hallucinogenic experience.

Salvinorin A primarily affects the kappa-opioid receptors in the brain, leading to a wide range of effects including altered perception, euphoria, and intense visual hallucinations. It has a unique mechanism of action compared to other hallucinogens.

Salvinorin A doesn't significantly impact heart rate or blood pressure.

Salvinorin A has analgesic and anti-inflammatory properties, suggesting potential therapeutic value for managing chronic pain.

Despite its unique mechanism, Salvinorin A can cause adverse reactions in some individuals, often manifesting as paranoia, hallucinations, and other psychotic-like symptoms, days after use.

Tolerance to Salvinorin A doesn't develop with repeated use; in fact, users often report needing higher doses and intensifying effects.

Withdrawal symptoms from Salvinorin A are typically mild, often including headache, irritability, and insomnia. However, prolonged heavy use can lead to more severe symptoms like nausea, vomiting, and stomach pain.

More research is needed to understand the long-term effects of Salvinorin A on the brain and body, as well as its mechanism of action. Its unique properties and potential risks still need further exploration.

Salvinorin A has a wide range of effects, including altered perception, euphoria, and intense visual hallucinations. It can be a profound experience for some, but also cause anxiety and disorientation in others.

Salvinorin A is a potent psychoactive substance with both promising potential and risks. It's important to approach it with caution and awareness of its potential effects.

Dissociative anesthetics, like PCP and ketamine, cause amnesia for events that occur while intoxicated, affecting memory formation.

PCP's impact on memory is more disruptive than LSD, THC, opioids, and many other psychoactive drugs.

Long-term ketamine use causes cognitive impairments, particularly with episodic memory, semantic memory, procedural learning, and working memory manipulation.

PCP and ketamine can induce symptoms of disordered thinking, resembling aspects of schizophrenia.

Despite their name, dissociative anesthetics don't induce hallucinations; they mainly cause relaxation, sedation, numbness, and euphoria.

Dissociative anesthetics are unique in their action; animals trained to recognize them don't generalize to other drug classes (stimulants, depressants, hallucinogens).

Tolerance develops to PCP with daily use, requiring higher doses to achieve the same effect.

Animal research suggests PCP withdrawal symptoms, including vocalizations, grinding teeth, diarrhea, sleep disturbances, anxiety, tremors, memory problems, and depression-like symptoms.

Tolerance can also develop to the analgesic effects of dissociative anesthetics, meaning they might become less effective at relieving pain over time.

Dissociative anesthetics have a unique stimulant property, with animals responding specifically only to other drugs that block NMDA receptors like dextromethorphan.

PCP, also known as "angel dust", is a synthetic drug that was initially marketed as an anesthetic but was withdrawn due to adverse effects like delirium and agitation.

Ketamine is a dissociative anesthetic that was developed as a safer alternative to PCP. It's used in veterinary medicine and human medicine for anesthesia and pain management.

PCP and ketamine have diverse routes of administration, including oral ingestion, snorting, smoking, and injection, making it a versatile and dangerous drug.

PCP and ketamine affect the nervous system by blocking NMDA receptors, a type of glutamate receptor vital for learning and memory. This blockage leads to the characteristic dissociative effects.

PCP and ketamine have diverse psychological effects that can range from euphoria and dissociation to paranoia and psychosis.

The duration of PCP and ketamine effects varies depending on the route of administration. Typically, a typical dose's effects last for several hours.

PCP and ketamine are classified as dissociative anesthetics because they alter perception, memory, and body awareness, leading to a disconnected feeling.

PCP and ketamine can cause physical dependence and withdrawal symptoms, especially in individuals who use them frequently.

The rewarding effects of PCP and ketamine are linked to their influence on dopamine release in brain regions associated with pleasure and motivation.

PCP and ketamine can have long-term effects on cognitive functions and brain health, emphasizing the importance of avoiding their use.

PCP and ketamine are often associated with violence, but this is a misconception. While large doses can cause disorientation and agitation, leading to injury, the drugs themselves don't promote violence.

Long-term ketamine use can alter the brain's structure and function, potentially leading to lasting neurological issues.

Ketamine use during pregnancy can harm the developing fetus, leading to growth problems, premature birth, and potential neurological issues in the child.

A lethal dose of ketamine is about 40 times higher than the normal effective dose, but co-use of depressants like alcohol increases the risk of fatal overdose.

Ketamine and PCP are not known to damage vital organs like the heart or liver.

Chronic ketamine use leads to long-term neurological changes in the brain, potentially affecting memory, learning, and other cognitive functions.

The combination of ketamine or PCP with central nervous system depressants like alcohol or barbiturates significantly increases the risk of lethal overdose.

PCP and ketamine are classified as dissociative anesthetics, meaning they can disrupt a person's sense of self and their surroundings. High doses can lead to a severe psychotic state.

PCP and ketamine can cause breathing difficulties, seizures, and coma when taken in high doses. These effects can be fatal.

Both PCP and ketamine can induce a temporary psychotic state, characterized by confusion, agitation, and hyperactivity. This can lead to self-harm or harm to others.