Depressant

Source: Wikipedia, the free encyclopedia.
Not to be confused with depressogen.

Colloquially known as "downers", depressants or central depressants are

drugs that lower neurotransmission levels, or depress or reduce arousal or stimulation in various areas of the brain.[1] Depressants do not change the mood or mental state of others. Stimulants, or "uppers", increase mental or physical function, hence the opposite drug class from depressants are stimulants, not antidepressants
.

Depressants are widely used throughout the world as

opioids. Gabapentinoids like gabapentin and baclofen are depressants and have anticonvulsant, and anxiolytic effects. Most anticonvulsants like Lamotrigine and Phenytoin are depressants. Carbamates are depressants that are similar to barbiturates
.

Depressants exert their effects through a number of different pharmacological mechanisms, the most prominent of which include facilitation of

GABA and inhibition of glutamatergic or monoaminergic activity. Other examples are chemicals that modify the electrical signaling inside the body, the most prominent of which are bromides and channel blockers
.

Indications

Depressants are used medicinally to relieve the following symptoms:

Types

hard liquor
", roughly eight times more alcoholic than beer

Alcohol

Main articles: Alcoholic beverage, Ethanol, and Blood alcohol content

An

spirits (distilled beverages). They are legally consumed in most countries around the world. More than 100 countries have laws regulating their production, sale, and consumption.[2]

The most common way to measure intoxication for legal or medical purposes is through

dL of blood (i.e., mass per volume is used there).[3]

Barbiturates

Main article: Barbiturate

Barbiturates are effective in relieving the conditions that they are designed to address (insomnia, seizures). They are also commonly used for unapproved purposes, are physically addictive, and have serious potential for

overdose. By the late 1950s, concerns over the mounting social costs associated with barbiturates, which were beginning to overshadow their perceived medical benefits, prompted a concerted effort to find alternative medications. Most people still using barbiturates today do so in the prevention of seizures or in mild form for relief from the symptoms of migraines.

Xanax (alprazolam
) 2 mg tri-score tablets

Benzodiazepines

Main article: Benzodiazepine
See also: Nonbenzodiazepine

A

Hoffmann–La Roche, who has also marketed the benzodiazepine diazepam
(Valium) since 1963.

Benzodiazepines enhance the effect of the

alcohol withdrawal, and as a premedication
for medical or dental procedures. Benzodiazepines are categorized as either short-, intermediate-, or long-acting. Short- and intermediate-acting benzodiazepines are preferred for the treatment of insomnia; longer-acting benzodiazepines are recommended for the treatment of anxiety.

In general, benzodiazepines are safe and effective in the short term, although cognitive impairments and

elderly are at an increased risk of experiencing both short- and long-term adverse effects
.

There is controversy concerning the safety of benzodiazepines in pregnancy. While they are not major

Beers List
, which is significant in clinical practice.

Cannabis

Main article: Cannabis

cannabinoids causes an inhibition of GABA, the exact opposite of what central nervous system depressants do.

Carisoprodol
tablets

Carbamates

Main article: Carbamate

tranquilizers" that are synthesized from urea.[7] Carbamates have anxiolytic,[8] muscle relaxant,[8] anticonvulsant,[9] hypnotic,[8] antihypertensive,[10] and analgesic effects. They have other uses like muscle tremors, agitation, and alcohol withdrawal. Their muscle relaxant effects are useful for strains, sprains, and muscle injuries combined with rest, physical therapy, and other measures.[8] The effects, synthesis, and mechanism of action of Carbamates are very similar to barbiturates.[11]
There are many different types of Carbamates: some only produce anxiolytic and hypnotic effects while some only have anticonvulsant effects.

overstimulation, and dependence. Uncommon but potentially severe adverse reactions include hyper sensitivity reactions such as Stevens Johnson syndrome, embryo-fetal toxicity, stupor, and coma. Carbamates are fatal in overdose, which is why many have been replaced with benzodiazepines. It is not recommended to use most Carbamates like Carisoprodol for a long time as physical and psychological dependence does occur.[12]

Meprobamate, which metabolizes to Carisoprodol, was launched in 1955. It quickly become the first blockbuster psychotropic drug in America, becoming popular in Hollywood and gaining fame for its seemingly miraculous effects. It has since been marketed under more than 100 trade names, including Amepromat, Quivet, and Zirpon. Carisoprodol, which is still used mainly for its muscle relaxant effects, can potentially abuse. Its mechanism of action is very similar to barbiturates, alcohol, methaqualone, and benzodiazepines. Carisoprodol allosterically modulates and directly activates the human α1β2γ2 GABAAR (GABAA) in the central nervous system, similar to barbiturates. This causes chloride channels to open, allowing chloride to flood into the neuron. This slows down communication between neurons and the nervous system.[13] Unlike benzodiazepines, which increase the frequency of the chloride channel opening, Carisoprodol increases the duration of channel opening when GABA is bound.[14][15] GABA is the main inhibitory neurotransmitter in the nervous system, which causes its depressant effects.

Carbamates are fatal in overdose. Symptoms are similar to a barbiturate overdose and typically include

respiratory depression). An overdose is more likely to be fatal when mixed with another depressant that suppresses breathing
.

Physical and

psychological dependence does happen with long term use of Carbamates; particularly Carisoprodol. Today Carisoprodol is only used in the short-term for muscle pain, particularly back pain. Discontinuation after long-term use could be very intense and even possibly fatal. Withdrawal can resemble barbiturate, alcohol, or benzodiazepine withdrawal, as they all have a similar mechanism of action. Discontinuation symptoms include confusion, disorientation, delirium, hallucinations (auditory & visual), insomnia, decreased appetite, anxiety, psychomotor agitation, pressured speech, tremor, tachycardia, and seizures, which could be fatal.[16]

Carbamates gained widespread use in the 1950s, alongside barbiturates. While their popularity has gradually waned due to concerns over overdose and dependence potential, newer derivatives of carbamates continue to be developed. Among these is

Schedule IV substance in the United States. Famous martial artist and actor Bruce Lee died due to an allergic reaction to meprobamate
.

Approved

Although a drug may be approved, that does not necessarily mean it is still being used today.

Not approved

Gabapentinoids

Main article:
Gabapentinoids
Voltage gated calcium channel
Baclofen
tablets

non-selective when they bind to the calcium channels complex. They act on the α2δ site to lower the release of many excitatory and pro-nociceptive neurochemicals including glutamate, substance P, calcitonin gene-related peptide (CGRP), and more.[18][19][20]

Gabapentinoids are absorbed from the intestines mainly by the

Large neutral amino acid transporter 1 (LAT1, SLC7A5) and the Excitatory amino acid transporter 3 (EAAT3). They are one of the few drugs that use these amino acid transporters. Gabapentinoids are structurally similar to the Branched-chained amino acids L-leucine and L-isoleucine, both of which also bind to the α2δ site. Branched-chained amino acids like l-leucine, l-isoleucine, and l-valine have many functions in the central nervous system. They modify large neutral amino acid (LNAA) transport at the blood–brain barrier and reduce the synthesis neurotransmitter of neurotransmitters derived from aromatic-amino acids, notably serotonin from tryptophan and catecholamines from tyrosine and phenylalanine.[21] This may be relevant to the pharmacology
of gabapentinoids.

Gabapentin was designed by researchers at

dihydropyridine class are used for hypertension weakly block α2δ.[30]

Gabapentinoids have anxiolytic,

vestibular disorders, Ménière's disease, dizziness, for the prevention of motion sickness, and for the prevention of anxiety before or after surgical procedures or painful diagnostic tests.[48] Phenibut, like other GABA B agonists, is also sometimes used by body builders to increase the human growth hormone
.

Reuters reported on 25 March 2010 that "Pfizer Inc violated a United States racketeering law by improperly promoting the epilepsy drug Neurontin (gabapentin). Under the Racketeer Influenced and Corrupt Organizations Act, the penalty is automatically tripled, so the finding will cost Pfizer $141 million." The case stems from a claim from Kaiser Foundation Health Plan Inc. that "it was misled into believing Neurontin was effective for off-label treatment of migraines, bipolar disorder and other conditions. Pfizer argued that Kaiser physicians "still recommend the drug for those uses", and that "the insurer's website also still lists Neurontin as a drug for neuropathic pain."

In some cases, gabapentinoids are abused and provide similar effects to alcohol, benzodiazepines and gamma-hydroxybutyric acid (GHB).[49][50][51] The FDA placed a black box warning on Neurontin (gabapentin), and Lyrica (pregabalin), for serious breathing problems.[52] Mixing gabapentinoids with opioids, benzodiazepines, barbiturates, GHB, alcohol, or any other depressant is potentially deadly.[53][54][55][56]

Common

side effects of gabapentinoids include drowsiness, dizziness, weakness, increased appetite, urinary retention, shortness of breath, involuntary eye movements (nystagmus), memory issues, uncontrollable jerking motions, auditory hallucinations, erectile dysfunction, and myoclonic seizures.[57][58]

An

anti-diabetic agents (thiazolidinediones). It is not known if they cause gingival enlargement like other calcium channel blockers. Gabapentinoids are excreted by the kidney mostly in their original form. Gabapentinoids can build up in the body when someone has renal failure. This usually presents itself as myoclonus and an altered mental state. It is unclear if it is safe to use gabapentinoids during pregnancy, with some studies showing potential harm.[65]

intrathecally or for long periods of time. If baclofen or phenibut is used for long periods of time it can resemble intense benzodiazepine, GHB or alcohol withdrawal. To minimize withdrawal symptoms, baclofen or phenibut should be tapered down slowly. Abrupt withdrawal from phenibut or baclofen could possibly be life-threatening because of its mechanism of action. Abrupt withdrawal can cause rebound seizures and severe agitation.[71][70]

Not approved:

Endogenous (not Gabapentinoids), endogenous BCAA amino acids that bind to α2δ):

Other α2δ ligands:[72][73]

Gamma-Hydroxybutyric acid

Main article: Gamma-Hydroxybutyric acid
GABA analogues
GABA analogues
Severity of GHB withdrawal syndrome
Severity of GHB withdrawal syndrome
GHB that is used to treat alcohol addiction in Italy.
GHB that is used to treat alcohol addiction in Italy.

Gamma-Hydroxybutyric acid or "GHB" is a GABA analogue that is a natural occurring neurotransmitter and depressant drug.[75][76][77] It is also naturally found in small amounts some alcoholic beverages alongside ethanol.[78] GHB is the prototypical substance among a couple of GHB receptor modulators.[79]

GHB has been used as a general anesthetic[80][81] and as a treatment for cataplexy,[82][83] narcolepsy,[82][84] and alcoholism.[85][86][87][88] The sodium salt of GHB, sodium oxybate, is commonly used today for narcolepsy,[89] sudden muscle weakness,[90] and excessive daytime sleepiness. It is sold under the brand name Xyrem.[91][92][89]

As a depressant, GHB would worsen narcolepsy and muscle weakness. But in low doses GHB mainly affects the GHB receptor,[93][94] an excitatory receptor that releases dopamine and glutamate[95] giving GHB stimulant effects, the opposite of a depressant. But in large doses GHB activates the GABAB receptor, an inhibitory receptor in the central nervous system, which overpowers the excitatory effects, thus causing central nervous system depression.[96][97] Some antipsychotics are agonists of the GHB receptor.[98][99][100]

GHB can usually be found in either as

respiratory depression, seizures, or coma.[96][112][113]

GHB is used illegally as an

Schedule I substance in the United States and Canada and other countries. Xyrem, which is GHB in its sodium form, is Schedule III in the United States, Canada and other countries.[91][104]

In low doses, GHB mainly binds to the

glutamate.[95] GHB can also causes absence seizures;[112][120][121] the mechanism is currently not known but it is believed to be due to interactions with the GABAB receptor.[120] It is being investigated if endogenous GHB is responsible for non-convulsive seizures in humans.[112][122]

GHB withdrawal is very intense.[123] Physical dependence develops quickly. It is also highly psychologically addictive. It shares some similarities with the withdrawal of gabapentinoids phenibut and baclofen due to the activation of the GABAB receptor. It features a typical depressant withdrawal syndrome that mimics alcohol withdrawal.[124] Symptoms include delirium, tremor, anxiety, tachycardia, insomnia, hypertension, confusion, sweating, severe agitation which may require restraint,[125] auditory and visual hallucinations and possibly death from tonic-clonic seizures.[1][126][124][127][128][129]

Baclofen and phenibut are very effective for withdrawal and are preferred by patients over benzodiazepines for treatment of withdrawal.[127]

GHB receptor modulators:

GHB receptor agonists:

- Calcium Oxybate, Magnesium Oxybate, Sodium Oxybate (Xyrem), Potassium Oxybate. Xywav is a mixture of all these salts.

Prodrugs that metabolize into GHB:

  • γ-Hydroxyvaleric acid (GHV)

-

gamma-Valerolactone, γ-Valerolactone
(GVL) prodrug to GHV

GHB receptor antagonists:

Some GHB receptors modulators only bind to the GHB receptor, while others bind to both the GHB and GABAB receptors

Nonbenzodiazepines

Zolpidem
Zolpidem
Zaleplon
Zaleplon

benzodiazepine site of the GABAA receptor, the chief inhibitory receptor of the central nervous system
just like benzodiazepines, but a molecular level, they are structurally unrelated.

Nonbenzodiazepines bind to the benzodiazepine of the GABAA receptor site to keep the chloride channel open.[131] This causes chloride in the intercellular area to flood into the neuron.[132] Since chloride has a negative charge it causes the neuron to rest and cease firing. This results in a relaxing and depressant effect in the central nervous system.

Common nonbenzodiazepines like Zolpidem and Zopiclone are extremely effective for insomnia but carry many risks and side effects. Sleeping pills, including zopiclone, have been associated with an increased risk of death.

Adverse reactions as follows: "taste disturbance (some report a metallic like taste); less commonly nausea, vomiting, dizziness, drowsiness, dry mouth, headache; rarely amnesia, confusion, depression, hallucinations, nightmares; very rarely light headedness, incoordination, paradoxical effects, and sleep-walking also reported". Some users of nonbenzodiazepines have sleep-walked and committed murders or have been involved in motor vehicle accidents. Unlike benzodiazepines, nonbenzodiazepines have a risk of hallucinations and sleep-walking. Like benzodiazepines, they can cause anterograde amnesia.

Nonbenzodiazepines should not be discontinued abruptly if taken for more than a few weeks due to the risk of

benzodiazepine equivalent dose of a long-acting benzodiazepine (such as chlordiazepoxide or more preferably diazepam) can be tried followed by a gradual reduction in dosage. In extreme cases and, in particular, where severe addiction and/or abuse is manifested, an inpatient detoxification may be required, with flumazenil
as a possible detoxification tool.

Opioids/Opiates

Main article:
Opioids
5mg Oxycodone hard capsules
Oxycodone is a semi-synthetic prescription opioid.
Papaver somniferum
Papaver somniferum
The rostromedial tegmental nucleus is located in the midbrain (pictured above) of the brainstem. Release of dopamine in the RMTG characterizes the euphoria/reinforcement of opioids.
The rostromedial tegmental nucleus is located in the midbrain (pictured above) of the brainstem. Release of dopamine in the RMTG characterizes the euphoria/reinforcement of opioids.

Opioids are substances that act on

pain relief, including anesthesia. Opioids also cause euphoria
and are highly abused.

Opioids and Opiates are not the same. Opiates refer to natural opioids such as morphine and codeine. Opioids refer to all natural, semisynthetic, and synthetic opioids, like heroin and oxycodone.

Contrary to popular misconception, opioids are not depressants in the classical sense.[4] They do produce central nervous system depression, but they also excite certain areas of the central nervous system. To remain true to the term 'depressant' – opioids cannot be classified as such. For opioid agonists and opium derivatives, these are classified differently. analgesic or narcotic correctly identifies these drugs. However, they do have depressant actions nonetheless.

There are three principal classes of opioid receptors,

δ (mu, kappa, and delta),[134] although up to seventeen have been reported, and include the ε, ι, λ, and ζ (Epsilon, Iota, Lambda and Zeta) receptors. Conversely, σ (Sigma) receptors are no longer considered to be opioid receptors because their activation is not reversed by the opioid inverse-agonist naloxone.The nociception opioid peptide receptor (NOP) (ORL1) is an opioid receptor which is involved in pain responses, anxiety, movement, reward, hunger, memory, and much more. It plays a major role in the development of tolerance to μ-opioid agonists.[135]

When "pain" occurs, a signal gets sent from the site of possible injury. This signal goes up the spinal cord into the brain where it is perceived as a negative emotion known as nociception or "hurt". In the central nervous system, the spine is connected to the brain by a structure called the brain stem.[136] The brain stem is the first part of the brain that develops in a mammal out of the neural crest. It is also the oldest part of the brain and controls many automatic functions such as consciousness, breathing, heart rate, digestion, and many more. Opioid receptors are specialized pain blocking receptors. They bind a wide range of hormones, peptides, and much more. Although they are found everywhere in the central nervous system, they are highly concentrated in the brain stem. Depending on the receptor, activation of them has the ability to stop pain from making its way to the brain and being perceived as pain. Hence opioids do not actually "stop" pain; they simply stop you from knowing you are in pain. Pain and the ability to modify it based on an organism's environment is an evolutionary advantage, and it has been shown that it can help an organism escape and survive certain situations where they may otherwise be immobilized due to pain and injury. The midbrain nuclei of the brain stem, with structures like the periaqueductal gray, reticular formation, and rostromedial tegmental nucleus, are responsible for the majority of the physical and psychological effects of endogenous and exogenous opioids.

The μ-opioid receptor is the responsible for the analgesic, euphoric, and adverse effects of opioids. The μ-opioid receptor is a G-protein coupled receptor. When the μ-opioid receptor is activated, it causes pain relief, euphoria, constipation, constricted pupils, itching, and nausea.[3] The μ-opioid is located in the gastrointestinal tract, which controls peristalsis. This causes constipation, which can be extremely problematic and distressing. Activation of this receptor also causes relaxation of voluntary and involuntary muscles which can cause side effects like trouble urinating and swallowing. The μ-opioid receptor can also reduce androgens, thus decreasing libido and sexual function. The receptor is also known to cause "musical anhedonia".[137]

The receptor plays a critical role in

mu opioid receptors and are present in the rostromedial shell of the nucleus accumbens on its spiny neurons
. This area has been called the "opioid eating site".

The μ-opioid receptor has many endogenous ligands including endorphin.[138]

Adverse effects of opioids (μ-opioid receptor)

Common and short term

Other

The Kappa receptor (KOR) is a G protein-coupled receptor located in the central nervous system. KOR is also a G-protein coupled receptor.[140] Humans and some other primates have a higher density of kappa receptors than most other animals. KOR is responsible for nociception, consciousness, motor control, and mood. Dysregulation of this receptor system has been implicated in alcohol and drug addiction.[4] The endogenous ligand for KOR is dynorphin. Activation of KOR usually causes dysphoria; hence the name dynorphin. The intoxicating plant, Salvia divinorum contains salvinorin A, an alkaloid that is a potent and selective κ-opioid (kappa-opioid) receptor agonist. This causes powerful hallucinations. Antagonizing the κ-opioid (kappa-opioid) receptor may be able to treat depression, anxiety, stress, addiction and alcoholism.[141]

The third receptor is the

G-protein coupled receptor, and its endogenous ligand is deltorphin. Activation of δ-opioid receptor (DOR) may have antidepressant effects. δ-opioid agonists can produce respiratory depression at very high doses; at lower doses, they have the opposite effect. High doses of an δ-opioid agonist can cause seizures, although not all delta agonists produce this effect.[142]
Activation of the delta receptor is usually stimulating instead of sedating like most opioids.

The nociception receptor is involved in the regulation of numerous brain activities, particularly instinctive emotional behaviors and pain.

gastrointestinal motility, anxiety, and the control of neurotransmitter release at peripheral and central sites.[144]

ion channels and receptors is a hallmark of a depressant. Without glutamate the pain signal gets "cut short" and cannot ascend a pathway and reach pain processing centers in the midbrain of the brainstem
.

An

pinpoint pupils and respiratory depression. Other symptoms include seizures and muscle spasms. Opioids activate μ-opioid receptors in specific regions of the central nervous system associated with respiratory regulation. They activate μ-opioid receptors in the medulla and pons. They are located in the brain stem connecting to the spine. This area has a high density of μ-opioid receptors as they block pain going up from spine into the brain. These areas are the oldest and most primitive parts of the brain. They control automatic functions such as breathing and digestion. Opioids stop this process and cause respiratory depression and constipation. The brain stem no longer detects carbon dioxide in the blood, so it does not initiate the inhalation reflex, usually resulting in hypoxia. Some overdose victims, however, die from cardiovascular failure
, or asphyxiation from choking on their vomit.

cold sweats
and diarrhea.

Opioids activate μ-opioid receptors in the

Psychostimulants also excite this pathway.[149][150]

Fentanyl is very commonly cut into other substances sold on the street.[7] Fentanyl is used to increase the potency of substances, thus making the user spend more money on the laced substance.[152][153] Codeine is a weaker natural opiate that is usually used for bronchitis, diarrhea, and post-operative pain. It is very easy to overdose on these substances, especially if you have no tolerance. It is recommended to get your drugs tested, and to carry Naloxone.

Natural Opiates (Papaver somniferum, Opium)

Semi-synthetic Morphinan Opioids:

Semi-synthetic Opioids are derived from the natural alkaloid thebaine.

Fully synthetic Opioids:

Others:

Mitragyna speciosa (Kratom) Indole alkaloid

Piperidinediones

Main article: Glutarimide
barbituratess
.

central nervous depressants. The Piperidinedione depressants, specifically Glutethimide, are positive modulators of the GABAA anion channel. The drug increases inhibitory GABAergic tone and causes neuro-inhibition of the cortical and limbic systems, observed clinically as a sedative-hypnotic effect.[11] Glutethimide is also a potent inhibitor of the CYP 2D6 enzyme in the liver. This enzyme is responsible for converting many drugs from beta blockers to antidepressants to opioids and opiates. Due to its effects on the conversion of opioids, it was highly abused and mixed with opioids like codeine. Codeine must be metabolized to morphine in the liver to have its psychoactive and analgesic
effects. Mixing codeine with the Piperidinedione Glutethimide allowed more codeine to be converted into morphine in the body; thus increasing its effect. These were known as "hits", "cibas and codeine", and "dors and 4s". Glutethimide was believed to be safer than barbiturates, but many people died from the drug. Demand was high in the United States at one point. Production of glutethimide was discontinued in the US in 1993 and in several eastern European countries, most notably Hungary, in 2006.

Glutethimide withdrawal is intense and resembles barbiturate withdrawal. It features hallucinations and delirium typical of a depressant withdrawal. In the 1970s, there were reports of

vasomotor instability, incessant crying, and general irritability
.

Glutethimide withdrawal featured severe agitation, tremor, and seizures which could be fatal.

Overdose causes stupor or coma and respiratory depression.

  • Methyprylon (Dimerin, Methyprylone, Noctan, Noludar)
  • Pyrithyldione (Presidon, Pyridion, Pyridione, Pyrithyldion, Pyrithyldione)
  • Piperidione (Ascron, Dihyprylon, Dihyprylone, Sedulon, Tusseval) (Withdrawan before approval)
  • Glutethimide (Doriden)

Quinazolinone

Main article: Quinazolinone
Methaqualone tablets
Nitromethaqualone structure

Quinazolinones are a class of depressants that are rarely used anymore. Quinazolinones have powerful sedative, hypnotic, and anxiolytic effects. Quinazolinone's structure is very similar to some antibiotics. Quinazolinone's main mechanism of action is binding to the GABAA receptor.

GABRA1 proteins on the GABAA receptor.[154] The anesthetic etomidate and Anticonvulsant loreclezole may also bind to this site.[154]

Overdosing on quinazolinone sometimes causes effects that are the opposite of quinazolinone-like sedation. The overdose consists of hyperreflexia, vomiting, kidney failure, delirium, hypertonia, coma, myoclonic twitches, somnolence, euphoria, muscular hyperactivity, agitated delirium, tachycardia, and tonic-clonic seizures. In 1982, 2,764 people visited US emergency rooms from overdosing on quinazolinones, specifically Methaqualone.[155] Mixing quinazolines with another depressant is possibly fatal. Death from a quinazolinone overdose is usually caused by death through cardiac or respiratory arrest. Overdose resembles barbiturate/carbamate overdose.

Quinazolinone

muscle spasms, and irritability.[156]

portmanteau, combining the words "quiet interlude". Methaqualone was discontinued in the United States in 1985, mainly due to its psychological addictiveness
, widespread abuse, and illegal recreational use. Nonbenzodiazepines, and benzodiazepines are now used to treat insomnia instead. Methaqualone is now a Schedule I substance. Some quinazolinone analogues are still sold online. They come with the risk of seizure.

Large doses of Methaqualone can cause euphoria,

Seconal. Billy Murcia, a drummer for the rock band New York Dolls, died at 21 when he drowned in a bathtub while overdosing on heroin and Methaqualone.[162]

Cloroqualone was a quinazolinone that bound to the GABAA and sigma-1 receptor. It had useful cough suppressant effects and weaker sedative effects than Methaqualone, but was ultimately withdrawn due to its potential for abuse and overdose.[163]

cyclooxygenase-1 enzyme, and possibly its agonist activity at both the Sigma-1 receptor and Sigma-2 receptor. Diproqualone is used primarily for the treatment of inflammatory pain associated with osteoarthritis and rheumatoid arthritis; it is used more rarely for treating insomnia, anxiety and neuralgia. Diproqualone is the only analogue of methaqualone that is still in widespread clinical use due to its useful anti-inflammatory and analgesic effects along with the sedative and anxiolytic actions common to other drugs of this class. There are still some concerns about the potential of diproqualone for abuse and overdose; it is sold not as a pure drug but as the camphosulfonate salt in combination mixtures with other medicines such as ethenzamide
.

central nervous system depressant
properties. It was highly abused, and had high risk for overdose. Users would snort or smoke the free base Etaqualone hydrochloride salt.

analogue of methaqualone.[164]

Nitromethaqualone is a quinazolinone depressant with ten times more hypnotic and sedative effects than Methaqualone.[165]

Quinazolinones:

Miscellaneous

Methods of intake

Combining multiple depressants can be very dangerous because the central nervous system's depressive properties have been proposed to increase exponentially instead of linearly.[166] This characteristic makes depressants a common choice for deliberate overdoses in the case of suicide. The use of alcohol or benzodiazepines along with the usual dose of heroin is often the cause of overdose deaths in opiate addicts.

See also

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External links
Retrieved from "https://en.wikipedia.org/w/index.php?title=Depressant&oldid=1218788108"