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Stimulant, SNDRI

Cocaine

Also called Coke, Coca, Crack, Blow, Girl, White, Snow, Nose Candy, Yayo, Perico, Gear, Chari

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Common dose · Insufflated30–60 mg PW
Onset3–10 minutes PW
Total10–90 minutes PW
After-effectsPsychological craving and compulsive redosing PW

Dosage

When sources disagree, both rows are shown as published. Nothing is averaged or merged.

Insufflated

SourceThresholdLightCommonStrongHeavy
PsychonautWiki5 mg PW10–30 mg PW30–60 mg PW60–90 mg PW90 mg+ PW
TripSit–20–50 mg TS50–100 mg TS100–150 mg TS150 mg+ TS

Bioavailability: 60–80%[65][66] PW

Intravenous

SourceThresholdLightCommonStrongHeavy
PsychonautWiki2 mg PW2–5 mg PW5–10 mg PW10–15 mg PW15 mg+ PW

Bioavailability: 100% PW

Oral

SourceThresholdLightCommonStrongHeavy
PsychonautWiki13 mg PW13–75 mg PW75–150 mg PW150–225 mg PW225 mg+ PW

Bioavailability: 33%[67] PW

Smoked

SourceThresholdLightCommonStrongHeavy
PsychonautWiki2.5 mg PW5–15 mg PW15–30 mg PW30–45 mg PW45 mg+ PW

Bioavailability: 90%[36] PW

Rapid onset. Depending on purity, dosage will vary TS

TripSit dose text

TripSit's factsheet also states its doses as text.

Insufflated Light: 20-50mg Common: 50-100mg Strong: 100-150mg Heavy: 150mg+ | NOTE: Depending on purity, dosage will vary TS

What dose are you on? (self-reported, unverified)
Read this first. These numbers come from anonymous visitors typing in a box. Nobody checks them. People misjudge, mistype, troll, or take untested products of unknown strength. They are not a dose guide and never override the sourced table above. They exist only so the sourced ranges can be compared with what people say they take. If you are deciding what to take, use the sourced table, start low, and read the risks section.
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Duration

Route · sourceOnsetCome-upPeakOffsetTotalAfter-effects
Insufflated · PsychonautWiki3–10 minutes PW5–12 minutes PW7.5–16 minutes PW10–25 minutes PW10–90 minutes PWPsychological craving and compulsive redosing PW
Intravenous · PsychonautWiki3–5 seconds PW1–2 minutes PW2–10 minutes PW1–5 minutes PW5–15 minutes PW–
Oral · PsychonautWiki30–40 minutes PW40–50 minutes PW60–180 minutes PW10–25 minutes PW120–240 minutes PW–
Smoked · PsychonautWiki3–5 seconds PW1–2 minutes PW2–10 minutes PW1–5 minutes PW5–15 minutes PW–

TripSit factsheet

Duration
1-1.5 hours TS
Aftereffects
1-4 hours TS
Onset
Rapid. TS

Mixing

Acute combinations: what happens when these are taken close together. Entries backed by a medical journal or agency are listed first.

Backed by medical journals

Awaiting sourcePeer-reviewed reports on acute combinations, from PubMed and the journals the harm reduction sites cite.

Other documented combinations

  • Dangerous ΑMT PW
  • Dangerous Opioids - Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest. PW
  • Dangerous Tramadol - Tramadol and stimulants both increase the risk of seizures. PW
  • Dangerous MAOIs - This combination is poorly explored. PW
  • Unsafe DOx - The combined stimulating effects of the two can lead to an uncomfortable body-load, while the focusing effects of cocaine can easily lead to thought loops. Coming down from cocaine while the DOx is still active can be quite anxiogenic. PW
  • Unsafe 25x-NBOMe - Cocaine and NBOMes both provide considerable stimulation. When combined they can result in severe vasoconstriction, tachycardia, hypertension, and in extreme cases heart failure. PW
  • Unsafe 2C-T-x - Cocaine and 2C-T-x both provide considerable stimulation. When combined they can result in severe vasoconstriction, tachycardia, hypertension, and in extreme cases heart failure. PW
  • Unsafe 5-MeO-xxT - The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics. PW
  • Unsafe DXM - Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues. PW
  • Unsafe PCP - This combination can easily lead to hypermanic states. PW
  • Unsafe Alcohol - Drinking while using stimulants is risky because the sedative effects of alcohol are reduced. These are what the body uses to gauge “drunkenness”. This typically leads to excessive drinking with greatly reduced inhibitions, high risk of liver damage and increased dehydration. They will also allow you to drink past a point where you might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel alcohol less. Cocaine is potentiated somewhat by alcohol because of the formation of cocaethylene. PW
  • Uncertain Mushrooms - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences. PW
  • Uncertain LSD - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences. PW
  • Uncertain DMT - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences. PW
  • Uncertain Mescaline - The focus and anxiety caused by stimulants is magnified by psychedelics and results in an increased risk of thought loops. PW
  • Uncertain 2C-x - The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics. A combination of the stimulating effects may be uncomfortable. PW
  • Uncertain Cannabis - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences. PW
  • Uncertain Ketamine - No unexpected interactions, though likely to increase blood pressure but not an issue with sensible doses. Moving around on high doses of this combination may be ill-advised due to the risk of physical injury. PW
  • Uncertain MXE - Stimulants taken with MXE can lead to hypermanic states much more easily, especially if sleep is avoided. PW
  • Uncertain Amphetamines - This combination of stimulants will increase strain on the heart. It is not generally worth it as cocaine has a mild blocking effect on dopamine releasers like amphetamine. PW
  • Uncertain MDMA - Cocaine blocks some of the desirable effects of MDMA while increasing the risk of a heart attack. PW
  • Uncertain Caffeine - Both stimulants, risk of tachycardia, hypertension, and in extreme cases heart failure. PW
  • Uncertain GHB - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the sedative may overcome the patient and cause respiratory arrest. Likewise the G can wear off and leave a dangerous concentration of cocaine behind. PW
  • Uncertain GBL - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the sedative may overcome the patient and cause respiratory arrest. Likewise the G can wear off and leave a dangerous concentration of cocaine behind. PW

TripSit combination chart

TripSit rates each pairing. Only pairings with a number carry a citation from TripSit. See the whole chart, with TripSit's note for every pairing.

Dangerous

amt TSmaois TSopioids TStramadol TS

Caution

2c-x TSamphetamines TScaffeine TScannabis TSdmt TSghb/gbl TSketamine TSlsd TSmdma TSmescaline TSmushrooms TSmxe TS

Low Risk & Synergy

Low Risk & No Synergy

ssris TS

Low Risk & Decrease

Risks and toxicity

Chronic cocaine use has been shown to lead to neurotoxicity, being associated with high morbidity and mortality rates. Its extended use or abuse does also cause short-term downregulation of neurotransmitters.[45][74][75] PW

The most potentially harmful physical effects of cocaine appear to be not neurological but cardiovascular. Severe cardiac adverse events, particularly sudden cardiac death, become a serious risk at high doses due to cocaine's blocking effect on cardiac sodium channels. Moreover, long-term cocaine use may result in cocaine-related cardiomyopathy.[76][77] PW

Regular cocaine insufflation, the most popular method of ingestion, can have extremely adverse effects on one's nostrils, nose, and nasal cavities. These include a loss of the sense of smell, nosebleeds, difficulty swallowing, hoarseness, or a chronically runny nose. PW

"Crack lung" is a term for various pulmonary diseases caused by smoking crack cocaine, and it can develop even after short-term or initial use. While crack lung is usually reversible with appropriate medical care and most people recover fully, in some cases—especially if complications arise—lasting lung damage may occur. PW

It is strongly recommended that one use harm reduction practices if using this substance. PW

Lethal dosage

Susceptible individuals have died from as little as 30 mg applied to mucous membranes, whereas addicts may tolerate up to 5 grams daily.[78] PW

Dependence and abuse potential

As with other stimulants, the chronic use of cocaine can be considered highly addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage. Addiction is a serious risk with heavy recreational cocaine use but is unlikely to arise from typical medical use. PW

Tolerance to many of the effects of cocaine develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). PW

Cocaine exhibits cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of cocaine all stimulants will have a reduced effect. PW

Despite evidence of brain structure and function changes in chronic users, a 2018 systematic review found limited support for widespread cognitive impairment caused by long-term cocaine use, suggesting that common assumptions about pervasive cognitive deficits may be overstated.[79] PW

Withdrawal symptoms

After taking cocaine on a regular basis, some users will become addicted. When the substance is discontinued immediately, the user will experience what has come to be known as a "crash" along with a number of other cocaine withdrawal symptoms including paranoia, depression, Decreased libido, anxiety, itching, mood swings, irritability, fatigue, insomnia, an intense craving for more cocaine, and, in some cases, nausea and vomiting. PW

These symptoms can last for weeks or, in some cases, months. Even after most withdrawal symptoms dissipate most users feel the need to continue using the drug; this feeling can last for years and may peak during times of stress. About 30-40% of cocaine addicts will turn to other substances such as medication and alcohol after giving up cocaine. PW⚠ PsychonautWiki itself has flagged this text: citation needed.

The misuse of cocaine has a high correlation with suicide. In those who use cocaine, the risk is greatest during the withdrawal phase.[80][81][82] PW

Psychosis

Cocaine has a similar potential to induce temporary psychosis with more than half of cocaine abusers reporting at least some psychotic symptoms at some point.[83][84] PW

Typical symptoms of sufferers include paranoid delusions that they are being followed and that their drug use is being watched accompanied by hallucinations that support the delusional beliefs. Delusional parasitosis with formication ("cocaine bugs") is also a fairly common symptom.[85] PW

Cocaine-induced psychosis shows sensitization toward the psychotic effects of the drug. This means that psychosis becomes more severe with repeated intermittent use.[86] PW

Testing

Detection
Saliva: 1 day, Urine: 4-5 days, Hair: up to 90 days TS
Marquis
Clear (No change) TS

Effects

Elevated moodIncrease in irritabilityhyper-inflated egoeuphoriastimulationraised heartratenumbing effects depending on ROAnausea (particularly at high doses) TS

Overview

Cocaine (also known as benzoylmethylecgonine, and informally as coke, cola, snow, blow, white, among others) is a classical stimulant substance of the tropane class. It is a naturally-occurring alkaloid extracted from the leaves of two coca plant species; namely Erythroxylum coca and E. novogranatense that are native to South America. The mechanism of action involves increasing levels of serotonin, dopamine, and norepinephrine in the brain.[1] PW⚠ PsychonautWiki itself has flagged this text: citation needed.

A highly popular, short acting CNS stimulant that works by blocking the reuptake of dopamine, serotonin, and norepinephrine. It is known to increase euphoria, confidence, sex-drive, focus, body temperature, and heart rate. Cocaine can cause severe vasoconstriction and is known to be cardiotoxic and have a high potential for compulsive redosing and addiction.[2–22] TS

Cocaine is a central nervous system (CNS) stimulant and tropane alkaloid, derived primarily from the leaves of two coca species native to South America: Erythroxylum coca and E. novogranatense. The leaves are processed into cocaine paste, a crude mixture of coca alkaloids, from which cocaine base is isolated and then converted to cocaine hydrochloride. Although total synthesis is possible, it is complex and not used for production. Historically, cocaine was a standard topical medication used as a local anesthetic with intrinsic vasoconstrictor properties. However, its high abuse potential, adverse effects, and cost have limited its medical use and led to its replacement by alternative medicines.[23–31] WP

Street cocaine is commonly snorted, injected, or smoked as crack cocaine; its effects last up to 90 minutes depending on the route of administration. Pharmacologically, cocaine acts as a serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI), producing reinforcing effects such as euphoria, increased alertness, concentration, libido, and reduced fatigue and appetite.[26][32–36] WP

Cocaine has numerous adverse effects. Acute use can cause vasoconstriction, tachycardia, hypertension, hyperthermia, or seizures, while overdose may lead to stroke, heart attack, or sudden cardiac death. It also produces a spectrum of psychiatric symptoms, including agitation, paranoia, anxiety, irritability, psychosis, hallucinations, delusions, violence, and suicidal or homicidal thinking. Prenatal exposure poses risks to fetal development. Chronic use may result in cocaine dependence, withdrawal symptoms, neurotoxicity, and nasal damage, including cocaine-induced midline destructive lesions.[26][32][37–48] WP

Coca cultivation and initial processing occur primarily in Latin America, especially in the Andes regions of Bolivia, Peru, and Colombia. Cultivation is expanding into Central America, including Honduras, Guatemala, and Belize. Violence linked to the cocaine trade continues to affect Latin America and the Caribbean and is expanding into Western Europe, Asia, and Africa as transnational organized crime groups compete globally. Cocaine remains the world's fastest-growing illicit drug market.[27][49–56] WP

Coca chewing dates back at least 8,000 years in South America. Large-scale cultivation occurred in Taiwan and Java prior to World War II. The cocaine boom—a sharp rise in illegal production and trade—began in the late 1970s and peaked in the 1980s. Cocaine is regulated under international drug control conventions, though its legal status varies nationally: several countries have decriminalized possession of small quantities.[57–64] WP

History

History

Coca leaves have been used by indigenous South Americans for thousands of years, both as a stimulant and for medicinal purposes.[87] WP

When the Spanish arrived in South America, they initially banned coca but soon legalized and taxed it after seeing its importance to local labor. The active ingredient was first isolated in 1855 by Friedrich Gaedcke and later refined by Albert Niemann, who named it "cocaine". In the late 1800s, cocaine became popular in Western medicine as a local anesthetic and was widely used in various products, including drinks and remedies. and James Leonard Corning demonstrated peridural anesthesia. However, due to its toxic effects and potential for abuse, safer alternatives eventually replaced it in medical practice.[29][88–93] WP

Large-scale coca cultivation and cocaine production occurred in Asia, on Taiwan (then known as Formosa) and Java (today part of Indonesia) before World War II.[58][59] WP

Since the 1980s, the cocaine trade was dominated by centralized, hierarchical drug cartels such as Medellín and Cali, along with their successors and early FARC factions. By the early 2000s, this model fragmented into a diverse network of global trafficking links, allowing South American cocaine production to easily supply markets in Europe, Africa, Asia, and Oceania through various routes.[94] WP

Pharmacology

Pharmacokinetics

The extent of absorption of cocaine into the circulatory system after nasal insufflation is similar to that after oral ingestion. The rate of absorption after nasal insufflation is limited by cocaine-induced vasoconstriction of capillaries in the nasal mucosa. Onset of absorption after oral ingestion is delayed because cocaine is a weak base with a pKa of 8.6, and is thus in an ionized form that is poorly absorbed from the gastric acid and easily absorbed from the alkaline duodenum. The rate and extent of absorption from inhalation of cocaine is similar or greater than with intravenous injection, as inhalation provides access directly to the capillary bed. The delay in absorption after oral ingestion may account for the popular belief that cocaine bioavailability from the stomach is lower than after insufflation. Compared with ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects. Snorting cocaine produces maximum physiological effects within 40 minutes and maximum psychotropic effects within 20 minutes. Physiological and psychotropic effects from nasally insufflated cocaine are sustained for approximately 40–60 minutes after the peak effects are attained.[65][155] WP

Cocaine crosses the blood–brain barrier via both a proton-coupled organic cation antiporter and (to a lesser extent) via passive diffusion across cell membranes. As of September 2022, the gene or genes encoding the human proton-organic cation antiporter had not been identified.[156–159] WP

Cocaine has a short elimination half-life of 0.7–1.5 hours and is extensively metabolized by plasma esterases and also by liver cholinesterases, with only about 1% excreted unchanged in the urine. The metabolism is dominated by hydrolytic ester cleavage, so the eliminated metabolites consist mostly of benzoylecgonine (BE), the major metabolite, and other metabolites in lesser amounts such as ecgonine methyl ester (EME) and ecgonine. Further minor metabolites of cocaine include norcocaine, p-hydroxycocaine, m-hydroxycocaine, p-hydroxybenzoylecgonine (pOHBE), and m-hydroxybenzoylecgonine.[32][160][161] WP

Depending on liver and kidney functions, cocaine metabolites are detectable in urine between three and eight days. Generally speaking benzoylecgonine is eliminated from someone's urine between three and five days. In urine from heavy cocaine users, benzoylecgonine can be detected within four hours after intake and in concentrations greater than 150 ng/mL for up to eight days later.[162] WP

Body fluids

Cocaine and its major metabolites may be quantified in blood, plasma, or urine to monitor for use, confirm a diagnosis of poisoning, or assist in the forensic investigation of a traffic or other criminal violation or sudden death. Most commercial cocaine immunoassay screening tests cross-react appreciably with the major cocaine metabolites, but chromatographic techniques can easily distinguish and separately measure each of these substances. When interpreting the results of a test, it is important to consider the cocaine usage history of the individual, since a chronic user can develop tolerance to doses that would incapacitate a cocaine-naive individual, and the chronic user often has high baseline values of the metabolites in his system. Cautious interpretation of testing results may allow a distinction between passive or active usage, and between smoking versus other routes of administration.[163] WP

Hair

Hair analysis can detect cocaine metabolites in regular users until after the sections of hair grown during the period of cocaine use are cut or fall out.[164] WP

Pharmacodynamics

Cocaine acts as a serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI). Cocaine increases levels of serotonin, norepinephrine, and dopamine in the synaptic cleft, leading to heightened post-synaptic activation, with dopamine contributing to euphoria and arousal, and the other monoamines enhancing additional effects.[34][35][165][166][167] WP

The pharmacodynamics of cocaine involve the complex relationships of neurotransmitters (inhibiting monoamine uptake in rats with ratios of about: serotonin:dopamine = 2:3, serotonin:norepinephrine = 2:5). The most extensively studied effect of cocaine on the central nervous system is the blockade of the dopamine transporter protein. Dopamine neurotransmitter released during neural signaling is normally recycled via the transporter; i.e., the transporter binds the transmitter and pumps it out of the synaptic cleft back into the presynaptic neuron, where it is taken up into storage vesicles. Cocaine binds tightly at the dopamine transporter forming a complex that blocks the transporter's function. The dopamine transporter can no longer perform its reuptake function, and thus dopamine accumulates in the synaptic cleft. The increased concentration of dopamine in the synapse activates post-synaptic dopamine receptors, which makes the drug rewarding and promotes the compulsive use of cocaine.[26][168][169] WP

Cocaine affects certain serotonin (5-HT) receptors; in particular, it has been shown to antagonize the 5-HT₃ receptor, which is a ligand-gated ion channel. An overabundance of 5-HT₃ receptors is reported in cocaine-conditioned rats, though 5-HT₃'s role is unclear. The 5-HT₂ receptor (particularly the subtypes 5-HT2A, 5-HT2B and 5-HT2C) are involved in the locomotor-activating effects of cocaine.[170][171] WP

Cocaine has been demonstrated to bind as to directly stabilize the DAT transporter on the open outward-facing conformation. Further, cocaine binds in such a way as to inhibit a hydrogen bond innate to DAT. Cocaine's binding properties are such that it attaches so this hydrogen bond will not form and is blocked from formation due to the tightly locked orientation of the cocaine molecule. Research studies have suggested that the affinity for the transporter is not what is involved in the habituation of the substance so much as the conformation and binding properties to where and how on the transporter the molecule binds.[172] WP

Conflicting findings have challenged the widely accepted view that cocaine functions solely as a reuptake inhibitor. To induce euphoria an intravenous dose of 0.3-0.6 mg/kg of cocaine is required, which blocks 66-70% of DAT in the brain. Re-administering cocaine beyond this threshold does not significantly increase DAT occupancy but still results in an increase of euphoria which cannot be explained by reuptake inhibition alone. This discrepancy is not shared with other dopamine reuptake inhibitors like bupropion, sibutramine, mazindol or tesofensine, which have similar or higher potencies than cocaine as dopamine reuptake inhibitors. Furthermore, a similar response-occupancy discrepancy has been observed with methylphenidate, which also stabilizes the dopamine transporter in an open outward-facing conformation. These findings have evoked a hypothesis that cocaine may also function as a so-called "DAT inverse agonist" or "negative allosteric modifier of DAT" resulting in dopamine transporter reversal, and subsequent dopamine release into the synaptic cleft from the axon terminal in a manner similar to but distinct from amphetamines.[173–176] WP

Sigma receptors are affected by cocaine, as cocaine functions as a sigma ligand agonist. Further specific receptors it has been demonstrated to function on are NMDA and the D₁ dopamine receptor.[177][178] WP

Cocaine also blocks sodium channels, thereby interfering with the propagation of action potentials; thus, like lignocaine and novocaine, it acts as a local anesthetic. It also functions on the binding sites to the dopamine and serotonin sodium dependent transport area as targets as separate mechanisms from its reuptake of those transporters; unique to its local anesthetic value which makes it in a class of functionality different from both its own derived phenyltropanes analogues which have that removed. In addition to this, cocaine has some target binding to the site of the κ-opioid receptor. Cocaine also causes vasoconstriction, thus reducing bleeding during minor surgical procedures. Recent research points to an important role of circadian mechanisms and clock genes in behavioral actions of cocaine.[76][179–182] WP⚠ Wikipedia itself has flagged this text: unreliable medical source?.

Cocaine is known to suppress hunger and appetite by increasing co-localization of sigma σ₁R receptors and ghrelin GHS-R1a cell surface receptors, thereby increasing ghrelin-mediated signaling of satiety and possibly via other effects on appetitive hormones.[183][184] WP

Cocaine effects, further, are shown to be potentiated for the user when used in conjunction with new surroundings and stimuli, and otherwise novel environs.[185] WP

Chemistry

Formula
C17H21NO4 PC
CAS number
50-36-2 PC
Molar mass (g/mol)
303.35 PC
IUPAC name (computed by PubChem)
methyl (1R,2R,3S,5S)-3-benzoyloxy-8-methyl-8-azabicyclo[3.2.1]octane-2-carboxylate PC
SMILES
CN1[C@H]2CC[C@@H]1[C@H]([C@H](C2)OC(=O)C3=CC=CC=C3)C(=O)OC PC
InChIKey
ZPUCINDJVBIVPJ-LJISPDSOSA-N PC
PubChem CID
446220

User reports

Erowid erowid.org

Listings

Erowid Experience Vault listing TS

Link as published on TripSit's factsheet.

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Pop culture

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References

  1. Other Aggrawal, A. Narcotic Drugs. 1995
  2. Journal / agency Rhabdomyolysis associated with cocaine abuse
  3. Journal / agency The beta-lactam antibiotic ceftriaxone inhibits physical dependence and abstinence-induced withdrawal from cocaine, amphetamine, methamphetamine, a
  4. Journal / agency Effects of concurrent use of alcohol and cocaine
  5. Journal / agency Cocaine-like neurochemical effects of antihistaminic medications
  6. Journal / agency Cocaine cardiotoxicity: a review of the pathophysiology, pathology, and treatment options
  7. Journal / agency Citalopram enhances cocaine's subjective effects in rats
  8. Journal / agency Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias
  9. Journal / agency High cocaine dosage decreases neurogenesis in the hippocampus and impairs working memory
  10. Journal / agency The effects of combinations of intranasal cocaine, smoked marijuana, and task performance on heart rate and blood pressure
  11. Journal / agency Lack of cocaine-like discriminative-stimulus effects of σ-receptor agonists in rats
  12. Journal / agency Pregabalin reduces cocaine self-administration and relapse to cocaine seeking in the rat
  13. Journal / agency Cocaine potentiates MDMA-induced oxidative stress but not dopaminergic neurotoxicity in mice: implications for the pathogenesis of free radical-ind
  14. Journal / agency Effects of escitalopram on attentional bias to cocaine-related stimuli and inhibitory control in cocaine-dependent subjects
  15. Journal / agency Aminorex, a metabolite of the cocaine adulterant levamisole, exerts amphetamine like actions at monoamine transporters
  16. Journal / agency Long Withdrawal of Methylphenidate Induces a Differential Response of the Dopaminergic System and Increases Sensitivity to Cocaine in the Prefronta
  17. Journal / agency Cocaine tolerance and cross-tolerance
  18. Journal / agency Cocaethylene is as cardiotoxic as cocaine but is less toxic than cocaine plus ethanol
  19. Journal / agency Differential potentiation of L-tryptophan-induced head-twitch response in mice by cocaine and sertraline
  20. Journal / agency Cocaine contamination of United States paper currency
  21. Other A study suggests that having a history of cocaine and poly drug abuse can lead to acute open-angle glaucoma
  22. Other using cocaine while pregnant is dangerous for the fetus's health
  23. Harm reduction site Cocaine and crack drug profile | www.euda.europa.eu
  24. Other Cocaine - Alcohol and Drug Foundation
  25. Journal / agency The identification of coca (Erythroxylum species). Botanical Journal of the Linnean Society. doi:10.1111/j.1095-8339.1982.tb00368.x
  26. Journal / agency Pomara C, Cassano T, D'Errico S, Bello S, Romano AD, Riezzo I, Serviddio G. Data available on the extent of cocaine use and dependence: biochemistry, pharmacologic effects and global burden of disease of cocaine abusers. Current Medicinal Chemistry. 2012. doi:10.2174/092986712803988811 · PMID 22856655
  27. Harm reduction site Coca Cultivation in the Andean Region. June 2006
  28. Other De Precursores y Cocaína. 2016
  29. Journal / agency Latorre F, Klimek L. Does cocaine still have a role in nasal surgery?. Drug Safety. January 1999. doi:10.2165/00002018-199920010-00002 · PMID 9935273
  30. Journal / agency Bremner F. Apraclonidine Is Better Than Cocaine for Detection of Horner Syndrome. Frontiers in Neurology. 2019. doi:10.3389/fneur.2019.00055 · PMID 30804875 · PMC6371044
  31. Journal / agency Armbuster YC, Banas BN, Feickert KD, England SE, Moyer EJ, Christie EL, Chughtai S, Giuliani TJ, Halden RU, Graham JH, McCall KL, Piper BJ. Decline and Pronounced Regional Disparities in Medical Cocaine Usage in the United States. The Journal of Pharmacy Technology. December 2021. doi:10.1177/87551225211035563 · PMID 34790964 · PMC8592245
  32. Journal / agency Zimmerman JL. Cocaine intoxication. Critical Care Clinics. October 2012. doi:10.1016/j.ccc.2012.07.003 · PMID 22998988
  33. Other Cortés E, Metaal P. Smokable cocaine markets in Latin America and the Caribbean
  34. Journal / agency Azizi SA. Monoamines: Dopamine, Norepinephrine, and Serotonin, Beyond Modulation, "Switches" That Alter the State of Target Networks. The Neuroscientist. April 2022. doi:10.1177/1073858420974336 · PMID 33292070
  35. Journal / agency Cheng MH, Block E, Hu F, Cobanoglu MC, Sorkin A, Bahar I. Insights into the Modulation of Dopamine Transporter Function by Amphetamine, Orphenadrine, and Cocaine Binding. Frontiers in Neurology. 2015. doi:10.3389/fneur.2015.00134 · PMID 26106364 · PMC4460958
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