A depressant, or central depressant, is a drug that lowers neurotransmission levels, which is to depress or reduce arousal or stimulation, in various areas of the brain.[1] Depressants are also colloquially referred to as downers as they lower the level of arousal when taken. Stimulants or "uppers" increase mental and/or physical function, hence the opposite drug class of depressants is stimulants, not antidepressants.

Depressants are widely used throughout the world as prescription medicines and as illicit substances. Alcohol is a very prominent depressant. Alcohol can be and is more likely to be a large problem among teenagers and young adults. When depressants are used, effects often include ataxia, anxiolysis, pain relief, sedation or somnolence, and cognitive or memory impairment, as well as in some instances euphoria, dissociation, muscle relaxation, lowered blood pressure or heart rate, respiratory depression, and anticonvulsant effects. Depressants also act to produce anesthesia. Cannabis may sometimes be considered a depressant due to one of its components, cannabidiol. The latter is known to treat insomnia, anxiety and muscle spasms similar to other depressive drugs. However, tetrahydrocannabinol, another component, may slow brain function to a small degree while reducing reaction to stimuli, it is generally considered to be a stimulant and main psychoactive agent to sometimes cause anxiety, panic and psychosis instead. Other depressants can include drugs like Xanax (a benzodiazepine) and a number of opiates. Gabapentinoids like pregabalin and gabapentin are depressants and have anticonvulsant and anxiolytic effects.

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 these being bromides and channel blockers.


Depressants are used medicinally to relieve the following symptoms:



Distilled (concentrated) alcoholic beverages, sometimes called "spirit" or "hard liquor", roughly eight times more alcoholic than beer

An alcoholic beverage is a drink that contains alcohol (also known formally as ethanol), an anesthetic that has been used as a psychoactive drug for several millennia. Ethanol is the oldest recreational drug still used by humans. Ethanol can cause alcohol intoxication when consumed. Alcoholic beverages are divided into three general classes for taxation and regulation of production: beers, wines, and 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 blood alcohol content (also called blood alcohol concentration or blood alcohol level). It is usually expressed as a percentage of alcohol in the blood in units of mass of alcohol per volume of blood, or mass of alcohol per mass of blood, depending on the country. For instance, in North America a blood alcohol content of "0.10" or more correctly 0.10 g/dL means that there are 0.10 g of alcohol for every dL of blood (i.e., mass per volume is used there).[3]


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. In the late 1950s, when many thought that the social cost of barbiturates was beginning to outweigh the medical benefits, a serious search began for a replacement drug. 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

A benzodiazepine (sometimes colloquially "benzo"; often abbreviated "BZD") is a drug whose core chemical structure is the fusion of a benzene ring and a diazepine ring. The first such drug, chlordiazepoxide (Librium), was discovered accidentally by Leo Sternbach in 1955, and made available in 1960 by Hoffmann–La Roche, which has also marketed the benzodiazepine diazepam (Valium) since 1963.

Benzodiazepines enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABAA receptor, resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties; also seen in the applied pharmacology of high doses of many shorter-acting benzodiazepines are amnesic-dissociative actions. These properties make benzodiazepines useful in treating anxiety, insomnia, agitation, seizures, muscle spasms, 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 paradoxical effects such as aggression or behavioral disinhibition occasionally occur. A minority react reverse and contrary to what would normally be expected. For example, a state of panic may worsen considerably following intake of a benzodiazepine. Long-term use is controversial due to concerns about adverse psychological and physical effects, increased questioning of effectiveness, and, because benzodiazepines are prone to cause tolerance, physical dependence, and, upon cessation of use after long-term use, benzodiazepine withdrawal syndrome. Due to adverse effects associated with the long-term use of benzodiazepines, withdrawal from benzodiazepines, in general, leads to improved physical and mental health. The 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 teratogens, uncertainty remains as to whether they cause cleft palate in a small number of babies and whether neurobehavioural effects occur as a result of prenatal exposure; they are known to cause withdrawal symptoms in the newborn. Benzodiazepines can be taken in overdoses and can cause dangerous deep unconsciousness. However, they are much less toxic than their predecessors, the barbiturates, and death rarely results when a benzodiazepine is the only drug taken; however, when combined with other central nervous system depressants such as alcohol and opiates, the potential for toxicity and fatal overdose increases. Benzodiazepines are commonly misused and taken in combination with other addictive drugs. In addition, all benzodiazepines are listed in Beers List, which is significant in clinical practice.


Cannabis is often considered either in its own unique category or as a mild psychedelic.[4][5] The chemical compound tetrahydrocannabinol (THC), which is found in cannabis, has many depressant effects such as muscle relaxation, sedation, decreased alertness, and less tiredness.[citation needed] Contrary to the previous statement, activation of the CB1 receptor by cannabinoids causes an inhibition of GABA, the exact opposite of what central nervous system depressants do.[6]


Gabapentinoids are a unique class of depressants that selectively bind to the auxiliary α2δ subunit (CACNA2D1) and (CACNA2D2), site of certain VDCCs, and thereby act as inhibitors of α2δ subunit-containing Voltage-gated calcium channels. α2δ is nicknamed the "Gabapentin receptor". At physiologic or resting membrane potential, VDCCs are normally closed. They are activated (opened) at depolarized membrane potentials and this is the source of the "voltage-gated" epithet. Gabapentinoids bind to the α1 and α2 sites of the α2δ subunit family. Gabapentin is the prototypical gabapentinoid. The α2δ is found on L-type calcium channels, N-type calcium channels, P/Q-type calcium channels, and R-type calcium channels throughout the central and peripheral nervous systems. α2δ is located on presynaptic neurons and affects calcium channel trafficking and kinetics, initiates extracellular signaling cascades, gene expression and promotes excitatory synaptogenesis through thrombospondin 1 .[7] Gabapentinoids are not direct channel blockers, instead they disrupt the regulatory function of α2δ and its interactions with other proteins. Most of the effects of gabapentinoids are mediated by the high voltage activated N and P/Q-type calcium channels. P/Q-type calcium channels are mainly found in the cerebellum (Purkinje neurons), while N-type calcium channels are located throughout the central and peripheral nervous systems. N-type calcium channels are mainly responsible for the analgesic effects of gabapentinoids. Ziconotide, a non-gabapentinoid ω-conotoxin peptide binds to the N-type calcium channels and has analgesic effects 1000 times stronger than morphine. Gabapentinoids are selective for the α2δ site, but 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.[8][9][10]

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 amino acids L-leucine, and L-isoleucine, both of which also bind to the α2δ site. Gabapentinoids are also structurally similar to some Antihemorrhagic agents. 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 of neurotransmitters derived from aromatic-amino acids notably serotonin from tryptophan, and catecholamines from tyrosine and phenylalanine.[11] This may be relevant to the pharmacology of gabapentinoids.

Gabapentin was designed by researchers at Parke-Davis to be an analogue of the neurotransmitter GABA that could more easily cross the blood-brain barrier and was first described in 1975 by Satzinger and Hartenstein.[12][13] Gabapentin was first approved for epilepsy, mainly as an add-on treatment to partial seizures. Gabapentinoids are GABA analogues,[14] but they do not bind to the GABA receptors, do not convert into GABA or another GABA receptor agonist in vivo, and do not directly modulate GABA transport or metabolism.[15][16] Phenibut and baclofen, two structurally related compounds are exceptions as they mainly act on the GABA B receptor.[17][18] Also, gabapentin, but not pregabalin, has been found to activate Kvvoltage-gated potassium channels (KCNQ). Despite this, gabapentinoids mimic GABA activity by inhibiting neurotransmission.[19] Gabapentinoids prevent delivery of the calcium channels to the cell membrane, and disrupt interactions of α2δ with NMDA receptors, neurexins, and thrombospondins. Some calcium channel blockers of the dihydropyridine class used for hypertension weakly block α2δ.[20]

Gabapentinoids have anxiolytic, anticonvulsant, antiallodynic, and antinociceptive properties.[9][21][22] Pregabalin and gabapentin are used in epilepsy, postherpetic neuralgia, neuropathic pain associated with diabetic neuropathy, fibromyalgia, generalized anxiety disorder, and restless legs syndrome.[23][24][25][26][27][28] Pregabalin and gabapentin have many off-label uses including insomnia,[29] Alcohol and opioid withdrawal,[30] smoking cessation,[31] social anxiety disorder,[32] bipolar disorder,[33][34] attention deficit hyperactivity disorder,[35] chronic pain, hot flashes,[36] migraines and more. Baclofen is primarily used for the treatment of spastic movement disorders, especially in instances of spinal cord injury, cerebral palsy, and multiple sclerosis.[37] Phenibut is used in Russia, Ukraine, Belarus and Latvia to treat anxiety and to improve sleep, as in the treatment of insomnia.[38] It is also used for various other indications, including the treatment of asthenia, depression, alcoholism, alcohol withdrawal syndrome, post-traumatic stress disorder, stuttering, tics, 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.[38] Phenibut, like other GABA B agonists, is also sometimes used by body builders to increase 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).[39][40][41] The FDA placed a black box warning on Neurontin (gabapentin), and Lyrica (pregabalin), for serious breathing problems.[42] Mixing gabapentinoids with opioids, benzodiazepines, barbiturates, GHB, alcohol, or any other depressant is potentially deadly.[43][44][45][46]

Common side effects of gabapentinoids include drowsiness, dizziness, weakness, increased appetite, urinary retention, shortness of breath, involuntary eye movements (nystagmus), uncontrollable jerking motions, auditory hallucinations, erectile dysfunction, and myoclonic seizures.[47][48]

An overdose of gabapentinoids usually consists of severe drowsiness, severe ataxia, blurred vision, slurred speech, severe uncontrollable jerking motions, and anxiety.[49][50] Like most anticonvulsants, pregabalin and gabapentin have an increased risk of suicidal thoughts and behaviors.[51][52] Gabapentinoids, like all calcium channel blockers are known to cause angioedema.[53] Taking them with an ACE inhibitor can increase the toxic effects of Gabapentinoids.[54] They may also enhance the fluid-retaining effect of certain anti-diabetic agents (thiazolidinediones). It is unclear if it is safe to use Gabapentinoids during pregnancy with some studies showing potential harm.[55]

Physical or physiological dependence does occur during long-term use of gabapentinoids.[56] Following abrupt or rapid discontinuation of pregabalin and gabapentin people report withdrawal symptoms like insomnia, headache, nausea, diarrhea, flu-like symptoms, anxiety, depression, pain, hyperhidrosis, seizures, psychomotor agitation, confusion, disorientation, and gastrointestinal complaints.[57][58] Acute withdrawal from baclofen and phenibut may also cause auditory and visual hallucinations, and acute psychosis.[59][60]

  • Gabapentin (Neurontin)
  • Gabapentin Enacarbil (Horizant, Regnite)
  • Gabapentin Extended-Release (Gralise)
  • Pregabalin (Lyrica)
  • Phenibut (Anvifen, Fenibut, Noofen)
  • Baclofen (Lioresal)
  • Mirogabalin (Tarlige) (Japan Only)

Not approved:


Contrary to popular misconception, opioids are not depressants in the classical sense.[4] They do produce central nervous system depression, however, 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.


Methods of intakeEdit

Combining multiple depressants can be very dangerous because the central nervous system's depressive properties have been proposed to increase exponentially instead of linearly.[citation needed] 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 alsoEdit


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