Methaqualone
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Methaqualone — Quaaludes, ludes, Mandrax — is a synthetic depressant of the quinazolinone class. It was marketed as a safer alternative to barbiturates but proved comparably dangerous. Methaqualone is a positive allosteric modulator of GABAA receptors, producing its effects by enhancing inhibitory signaling at a transmembrane binding site shared with the anesthetic etomidate.[1]
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First synthesized in 1951 during antimalarial research in India,[2] methaqualone became the most commonly prescribed sedative in Britain by 1965 and a top-selling prescription drug in the United States.[3] Controlled studies confirmed abuse liability exceeding that of diazepam,[4] leading to US Schedule I classification in 1984 and the end of legal manufacture worldwide. It persists as a major illicit drug in South Africa, where it is smoked with cannabis as Mandrax.[5]
Subjective effects include sedation, muscle relaxation, euphoria, disinhibition, and anxiety suppression. The experience is defined by a distinctive tactile component — peripheral tingling in lips and fingertips, grounded in GABA-mediated modulation of somatosensory cortex[6] — that sets methaqualone apart from other GABAergic sedatives. Amnesia, impaired judgment, and compulsive redosing are characteristic unsought effects.
Methaqualone produces rapid physical dependence and carries significant overdose risk, with dose-dependent respiratory depression as the primary lethal mechanism.[7] Tolerance develops through dual pathways — receptor adaptation and accelerated liver metabolism[8] — driving dose escalation that narrows the safety margin; alcohol synergy persists for at least three days after a single dose.[9] The compound is well-characterized through decades of clinical use and 2024 cryo-EM structural studies,[10] though human pharmacokinetic parameters remain incompletely resolved.[11]
History[edit]
Discovery
Methaqualone was first synthesized in 1951 by Indra Kishore Kacker and Syed Husain Zaheer, who were screening quinazolinone derivatives for antimalarial activity at the Council for Scientific and Industrial Research in India.[2] The compound's sedative properties overshadowed its antimalarial potential. In 1955, M.L. Gujral marketed it in India as a purportedly non-addictive alternative to barbiturate sleeping pills.[2]
Clinical and commercial significance
Commercial distribution began in 1960 in the United Kingdom under the brand names Melsed, Melsedin, and Renoval.[3] By 1965, methaqualone was the most commonly prescribed sedative in Britain, and Quaalude — introduced by William H. Rorer Inc. — was climbing toward sixth-best-selling sedative in the United States.[12] In the UK, Mandrax combined methaqualone 250 mg with diphenhydramine 25 mg to potentiate the hypnotic effect,[13][12] a formulation that became dominant in British and South African markets.
Prohibition and persistence
The UK placed methaqualone under the Misuse of Drugs Act in 1971.[2] The United States classified it Schedule II in 1973 despite approximately 4 million prescriptions written that year,[3] then escalated to Schedule I in 1984, ending legal manufacture in most countries.[7][3] Despite global prohibition, methaqualone persists as one of South Africa's most prevalent illicit drugs, consumed as Mandrax through the "white pipe" method — crushed tablets smoked with cannabis.[14][5] In 2024, 17% of at-risk young women in Cape Town tested positive for methaqualone metabolites.[15]
The name Quaalude is a portmanteau of "quiet interlude," coined by manufacturer William H. Rorer Inc. Tablets imprinted with the number "714" became cultural shorthand for the drug, known colloquially as "Lemmons" or "714s".[12] In South Africa, the name Mandrax outlived the brand itself, becoming the generic term for all illicit methaqualone regardless of formulation or source.
Chemistry[edit]
Structural class
Methaqualone belongs to the quinazolinone chemical class — compounds built from a benzene ring fused to a pyrimidinone ring.[16] It is specifically a 2,3-disubstituted quinazolin-4-one: a methyl group at the 2-position and an ortho-tolyl group at the 3-position define its pharmacological identity. The ortho-methyl substituent restricts rotation around the N3–C(aryl) bond, a structural feature with implications for both stereochemistry and metabolism.
Moderate lipophilicity (XLogP 2.5[17]) allows efficient blood-brain barrier penetration, contributing to rapid CNS onset. Related compounds include the more potent research derivative PPTQ, which shares the same GABA-A binding site,[18] and the novel psychoactive substance SL-164, which appeared on unregulated markets around 2019.[19]
Molecular identity
| Molecular formula | C₁₆H₁₄N₂O |
| Molecular weight | 250.29 g/mol |
The molecule consists of a quinazolinone bicyclic system bearing a 2-methyl substituent and an ortho-tolyl group on N3.[17]
Stereochemistry
Methaqualone is achiral — it contains no classical stereocenters. However, the restricted rotation around the N3–C(aryl) bond produces atropisomerism: conformational mirror images arising from hindered bond rotation rather than a fixed asymmetric center. At body temperature, interconversion between forms is rapid enough that they cannot be separated.
The stereochemical relevance emerges in metabolism. Liver-enzyme-mediated hydroxylation proceeds with pronounced selectivity: the primary urinary metabolite, 4ʹ-hydroxymethaqualone, is excreted almost exclusively as a single enantiomer.[20] All five major hydroxylated metabolites display enantiomeric excess in human urine.[21]
Physical properties
| Appearance | White crystalline solid; bitter taste; little to no odor |
| Melting point (free base) | 120°C |
| Melting point (hydrochloride salt) | 255–265°C |
| Water solubility | 299.9 mg/L at 23°C |
| XLogP | 2.5 |
The free base is a moderately lipophilic solid with limited water solubility.[22] Its low pKa (2.54) means the molecule exists predominantly in neutral form at physiological pH, facilitating passive diffusion across biological membranes.
Pharmacology[edit]
Mechanism of action
Methaqualone acts as a positive allosteric modulator of GABAA receptors — the brain's principal inhibitory ion channels.[1] Rather than binding at the benzodiazepine, barbiturate, or neurosteroid sites, it occupies the transmembrane β(+)/α(−) subunit interface, the same site used by the general anesthetic etomidate.[1] A 2024 cryo-electron microscopy study resolved this interaction at atomic detail, showing that methaqualone inserts deeply into the intersubunit interface and widens the ion-conducting pore.[10]
Functional screening confirms a selective GABAergic mechanism — the compound shows negligible activity at other neurotransmitter receptors and transporters.[1] In animal models, methaqualone blocks GABA-deficiency seizures but not glycine-receptor seizures, confirming GABAergic specificity.[13] The dose-response hierarchy is orderly: anticonvulsant activity appears at low doses, muscle relaxation at moderate doses, and sedation at higher doses.[13]
Methaqualone's receptor profile is unusual among GABAergic drugs. It acts as a positive modulator at most synaptic GABAA subtypes but shows variable activity at extrasynaptic δ-containing receptors — ranging from negative modulation to superagonism depending on subunit composition.[1] This selectivity pattern has no parallel among clinically used GABAergic compounds.
Pharmacokinetics
Methaqualone is rapidly and nearly completely absorbed after oral administration, with approximately 99% absorbed within two hours.[12][23] Peak blood levels occur 2–3 hours after a 250 mg dose.[11] The compound distributes extensively into tissues with 70–90% binding to plasma proteins.[12]
The liver metabolizes more than 95% of each dose, with less than 5% excreted unchanged.[24] The primary metabolic pathway produces five hydroxylated metabolites and an N-oxide.[24][21] Metabolite excretion continues for at least 70 hours after a single dose.[24]
The half-life is disputed: controlled studies report approximately 10 hours,[11] while reference sources cite 20–60 hours. This discrepancy likely reflects two-compartment pharmacokinetics — a faster initial phase visible in controlled dosing, and a prolonged terminal phase detectable after overdose or chronic use.[25]
Neuroscience[edit]
Where it acts
Methaqualone's effects arise from enhanced GABAergic inhibition across multiple brain regions. In the cortex, GABA-A potentiation produces the dose-dependent progression from anxiolysis through sedation to unconsciousness.[1] In the somatosensory cortex, the compound alters the receptive fields of individual neurons — expanding or contracting the area of skin from which each neuron responds.[6]
This receptive-field modulation accounts for the tingling paresthesia concentrated in lips, fingertips, and other densely innervated body regions. The effect is sensitive to the benzodiazepine antagonist flumazenil, confirming GABAA involvement.[6] Motor-circuit GABAA receptors in the spinal cord and brainstem underlie the prominent muscle relaxation, which appears at doses below the sedative threshold.[13]
Why it matters
Methaqualone's euphoriant properties, confirmed in controlled comparison against diazepam,[4] implicate GABAergic modulation of the brain's reward circuitry. GABAA potentiation in the ventral tegmental area disinhibits dopamine-releasing neurons, increasing dopamine in the nucleus accumbens — the same reward mechanism engaged by benzodiazepines, barbiturates, and alcohol. Methaqualone's higher abuse liability may reflect its unusual engagement of extrasynaptic δ-containing receptors in reward circuits, a pathway inaccessible to benzodiazepines.[1]
The paradoxical convulsions seen in overdose[7] — unexpected for a GABA-enhancing compound — may involve selective depression of inhibitory interneurons or negative modulation at specific extrasynaptic receptor subtypes.[1] No neuroimaging or pharmacokinetic data exist for the smoked route, leaving the neural basis of the rapid-onset "white pipe" experience uncharacterized.
Subjective Effects[edit]
Methaqualone produces a warm, heavy sedation overlaid with a tactile euphoria that distinguishes it from other GABAergic depressants. The experience builds gradually over one to two hours into a state of deep physical relaxation and emotional disinhibition, where anxiety dissolves and social barriers lower. At higher doses, the sedative weight deepens toward hypnosis, amnesia sets in, and the capacity for coordinated movement deteriorates sharply. Set and setting exert moderate influence — the disinhibitory quality amplifies the social or solitary character of the environment.
Among sedatives, methaqualone most closely resembles high-dose benzodiazepine effects in its anxiolytic quality but diverges through stronger tactile euphoria and greater disinhibition — controlled comparison found it produced more euphoria than diazepam.[4] In overdose risk, it parallels barbiturates rather than benzodiazepines, lacking the latter's relative ceiling on respiratory depression.
Effect Grid
The full sedative-hypnotic profile manifests. Pronounced muscle relaxation and euphoria dominate the experience — controlled studies confirm methaqualone produces greater euphoria than diazepam at comparable doses. Anxiety suppression is strong. Disinhibition becomes prominent, with reduced impulse control and social inhibitions.
Tactile euphoria reaches its characteristic expression: peripheral tingling spreads across lips, fingertips, and genitalia. The body feels heavy and warm. Motor control impairment is clearly evident — gait becomes unsteady. Dizziness and vestibular distortion may occur. Sexual arousal enhancement is commonly reported, likely mediated by disinhibition rather than direct pharmacological effect.
Cognitive slowing is marked. Mild amnesia may develop for events during the experience. Compulsive redosing urge is present at this level — the desire to take more can be strong. Analysis suppression and thought deceleration are prominent. Do not drive or operate machinery.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Spatial disorientation · Visual acuity suppression · Proprioceptive distortion · Visual processing suppression · Internal hallucinations
Internal hallucinations
Dizziness · Body high · Physical fatigue · Sexual arousal enhancement · Bodily heaviness · Nystagmus (eye wobbles) · Nausea · Dry mouth · Constipation · Involuntary body movements · Trembling
Bodily heaviness · Nystagmus (eye wobbles) · Nausea · Dry mouth · Constipation · Involuntary body movements · Trembling
Cognitive euphoria · Focus suppression · Information processing suppression · Cognitive fatigue · Language suppression · Compulsive redosing urge · Confusion · Memory suppression · Motivation suppression · Thought disorganization · Aesthetic enhancement · Delusions of sobriety · Memory fragmentation · Amnesia · Delirium
Cognitive fatigue · Language suppression · Confusion · Memory suppression · Motivation suppression · Thought disorganization · Aesthetic enhancement · Delusions of sobriety · Memory fragmentation · Amnesia · Delirium
Timeline
Initial absorption begins. Subtle anxiolysis and a faint sense of calm may emerge as methaqualone crosses the blood-brain barrier. Effects are sub-threshold for most users.
Progressive sedation and muscle relaxation build. Peripheral tingling in lips and fingertips emerges — the characteristic somatosensory signature. Euphoria and anxiolysis become clearly perceptible.
Full sedative-hypnotic, euphoric, and tactile effect profile. Maximum disinhibition, muscle relaxation, and tactile euphoria. Motor impairment evident.
Gradual reduction in euphoria and sedation intensity. Residual muscle relaxation and drowsiness persist. Motor impairment slowly improves but remains present.
Residual drowsiness, cognitive slowing, and potential hangover. Alcohol sensitivity remains elevated for up to 3 days post-dose.
⚠ Do not drive or operate machinery for at least 24 hours after use.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- High
- Withdrawal
- Severefatal risk
- Tolerance buildup
- rapid
- Tolerance reset
- 10 days
- Physical
- High
- Psychological
- High
- Compulsive redosing
- High
- Dose escalation
- High
- Cross-tol.
- benzodiazepines · barbiturates · alcohol
Toxicity
Acute toxicity
No human lethal dose has been established through controlled data. The only published animal LD50 is 240 mg/kg (intraperitoneal, mouse),[27] which does not translate directly to human oral dosing. Doses exceeding 300 mg oral may produce dangerous effects in individuals without tolerance,[4] though this threshold lacks formal determination. safety citation needed
Overdose presentation
Methaqualone overdose presents with unconsciousness, respiratory depression, metabolic acidosis, and low potassium.[28] In a large case series of non-barbiturate hypnotic poisonings, unconsciousness and respiratory depression were the most common features, with 6 deaths among 349 cases.[29]
Unlike typical sedative overdoses, methaqualone toxicity can include convulsions, delirium, and hyperthermia.[7] These paradoxical features distinguish methaqualone overdose from the straightforward respiratory depression seen with barbiturates.
Respiratory depression
Dose-dependent respiratory depression is the primary life-threatening effect, shared with all GABA-A-enhancing drugs.[7] No antidote exists for clinical use. Naloxone (tested in mice at 10 mg/kg) partially reduced methaqualone lethality through an unclear mechanism, but it is not a standard treatment for methaqualone overdose in humans.[27]
Late post-overdose syndrome
A delayed withdrawal syndrome can emerge 1–3 weeks after methaqualone overdose: insomnia, restlessness, elevated REM sleep, seizures, and delirium.[26] This phenomenon is attributed to methaqualone persisting in brain tissue longer than in blood, with rapid development of physical dependence even following a single overdose event. Patients recovering from methaqualone overdose require monitoring well beyond the acute phase.
Psychological risks
The primary psychological risk is disinhibition-related harm. Suppression of prefrontal cortical function impairs judgment, decision-making, and impulse control.[7] In South Africa, methaqualone use is associated with sexual risk-taking, reduced ability to negotiate safer sex, increased HIV transmission,[30] and drug-facilitated sexual assault.[31]
Amnesia at higher doses creates blackout periods during which the user continues to act but cannot recall their behavior. Combined with disinhibition, this produces a high-risk profile for harm to self and others. The compound's high abuse liability[4] and compulsive redosing urge contribute to a pattern of escalating use.
Tolerance & dependence
Tolerance develops through two parallel mechanisms:
- Receptor adaptation: GABAA receptors adjust at the cellular level. In mice, continuous exposure produces measurable tolerance within 36 days.[32]
- Accelerated metabolism: Liver enzyme induction increases the rate of methaqualone breakdown. In clinically dependent patients, the resulting metabolic capacity was the highest measured for any drug-exposed group.[8]
This dual-mechanism tolerance drives dose escalation along two independent axes — the body both eliminates the drug faster and responds less at the receptor level.
Physical dependence has been confirmed in animals[32][33] and humans.[8] Withdrawal produces dangerous CNS hyperexcitability:
- Seizures — the most dangerous feature, comparable in risk to barbiturate or benzodiazepine withdrawal
- Insomnia and restlessness
- Elevated REM sleep and REM rebound effect
- Delirium and epileptic phenomena — documented 1–3 weeks post-exposure[26]
Cross-tolerance with barbiturates has been demonstrated: dependent animals show reduced sensitivity to pentobarbital.[34] Cross-tolerance extends broadly to other GABAergic depressants including benzodiazepines, alcohol, and GHB.
Methaqualone scores highly on abuse-liability assessments. Controlled studies found euphoria and abuse-liability scores significantly exceeding those of diazepam at tested doses.[4]
Drug interactions
Alcohol
The methaqualone-alcohol combination is the most dangerous and best-documented interaction. Alcohol reduces the minimum effective dose of methaqualone at the brain level, independent of any change in how the body processes either drug.[9] Separately, alcohol slows methaqualone elimination, prolonging its effects.[35]
In mice, methaqualone prolonged alcohol-induced unconsciousness by 269%.[27] The mechanism involves synergistic inhibition of a brain enzyme (Na-K-ATPase).[37]
GABAergic depressants
All GABAA-active drugs — benzodiazepines, barbiturates, GHB, anesthetics — carry additive or synergistic respiratory depression risk in combination with methaqualone.[7] Multiple GABA-enhancing drugs acting on different sites produce greater-than-additive suppression of breathing.
Baclofen
safety citation needed
Opioids
Opioid combination adds an independent pathway of respiratory depression via mu-opioid receptors in the brainstem — pharmacologically distinct from GABAA modulation, producing multiplicative rather than merely additive respiratory risk.[7]
Cannabis
The South African "white pipe" method combines methaqualone with cannabis.[14] No controlled studies of this combination exist. Cannabis effects are expected to overlay the sedative profile, and combustion products from the bottle-neck pipe method may contribute additional respiratory harm.
Contraindications
Absolute contraindications
- Concurrent use of other CNS depressants (alcohol, benzodiazepines, barbiturates, opioids, GHB, baclofen): synergistic respiratory depression risk renders any combination potentially lethal.[7]
- Respiratory insufficiency: pre-existing breathing impairment amplifies methaqualone's dose-dependent respiratory depression.
- Seizure disorders: paradoxical convulsions reported in overdose;[7] withdrawal from chronic use also lowers seizure threshold.
Relative contraindications
- Liver impairment: impaired liver function prolongs drug exposure and increases toxicity risk.
- Pregnancy: methaqualone crosses the placental barrier; pharmacokinetics are altered during pregnancy and labor.[38]
- History of substance use disorders: high abuse liability[4] and compulsive redosing make methaqualone high-risk for individuals with vulnerability to dependence.
- Concurrent CYP3A4 inhibitors: drugs that slow liver metabolism (ketoconazole, erythromycin, grapefruit juice) would be expected to increase methaqualone levels and toxicity risk. inferred
Harm Reduction[edit]
Forms & Identification
All current methaqualone is clandestinely manufactured[39] — no batch carries pharmaceutical-grade assurance of identity or purity. Tablets sold as Mandrax in South Africa routinely contain variable methaqualone content alongside unknown adulterants. Standard immunoassay drug screening panels may not detect novel quinazolinone analogs such as SL-164,[19] meaning a negative screen does not confirm the absence of related compounds. Quantitative analysis (GC-MS or LC-MS) provides the most reliable identification for any material suspected to contain methaqualone.
Guidelines
- Test any material before use with reagent kits and, where accessible, quantitative analysis.
- Start with the lowest plausible dose and wait at least 3 hours before considering redosing — oral absorption is complete but onset can be gradual.
- Do not combine with alcohol, opioids, benzodiazepines, or any other depressant.
- Arrange a sober sitter, particularly at doses above the threshold range.
- Eat a light meal beforehand to moderate absorption rate.
- Have a clear plan for where and how you will sleep — methaqualone produces strong sedation and motor impairment that escalates over the session.
- Be aware that the compulsive redosing urge is a documented pharmacological feature of this compound,[4] not a personal failing — decide on a dose before onset and remove remaining supply from immediate access.
Set & Setting
Methaqualone's pronounced disinhibition and amnesia potential make environmental control especially important. A familiar, low-stimulation setting with trusted companions reduces the risk of disinhibition-driven harm. The compound impairs motor coordination and judgment progressively — a sober companion who can monitor for respiratory depression and prevent dangerous behavior is strongly recommended. Avoid settings involving water, heights, driving, or any situation where impaired coordination could prove fatal.
Aftercare & integration. The day following methaqualone use is commonly marked by residual sedation, cognitive fog, and low mood. Prioritize sleep, hydration, and light nutrition. Avoid alcohol for at least three full days after use — the interaction window extends well beyond the subjective effects.[36]
If blackout periods occurred, consider that significant decisions or actions may have taken place without memory formation. Checking in with people present during the experience can help reconstruct events. Repeated experiences of amnesia or compulsive redosing are signals that the substance is producing harm regardless of subjective enjoyment — they warrant honest self-assessment and, if patterns persist, professional consultation.
Recovery & Support
Methaqualone withdrawal is medically dangerous — seizures are the most serious risk, comparable to barbiturate or benzodiazepine withdrawal. Do not attempt abrupt cessation after regular use without medical supervision. A medically supervised taper, typically using a long-acting benzodiazepine or phenobarbital under clinical guidance, is the standard approach to GABAergic depressant withdrawal.
Support resources include SAMHSA's National Helpline (US: 1-800-662-4357), local addiction medicine services, and peer support communities. In South Africa, where methaqualone remains widely available, the South African National Council on Alcoholism and Drug Dependence (SANCA) provides regional treatment referrals.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: The line between heavy sedation and dangerous overdose is narrow with methaqualone. Seek immediate medical help if any of the following occur:
- Breathing becomes slow, shallow, irregular, or stops
- The person cannot be woken by loud voice or firm sternum rub
- Lips, fingertips, or skin turn blue or gray
- Seizures or convulsions occur — unusual for most sedatives but documented with methaqualone[7]
- Body temperature rises sharply (hot, dry skin)
Immediate steps:
- 1. Call emergency services immediately.
- 2. Place the person in the recovery position (on their side, mouth angled downward) to prevent choking.
- 3. Monitor breathing continuously until help arrives.
- 4. Do NOT induce vomiting.
- 5. Do NOT leave the person alone.
What to tell the dispatcher: Name the substance (methaqualone, Mandrax, or Quaalude), estimated amount taken, time of ingestion, any other substances used (especially alcohol), and current symptoms. Good Samaritan laws in many jurisdictions protect callers from prosecution.
Reversal agents: No established antidote exists for methaqualone overdose. Treatment is supportive — airway management and monitoring.
Legal Status[edit]
Methaqualone is prohibited in most jurisdictions worldwide. Initially marketed as a prescription sedative in the 1960s, recognition of its abuse potential led to international scheduling under the United Nations Convention on Psychotropic Substances and national prohibition in all major markets.[3] No jurisdiction currently permits therapeutic use. Legal manufacture ceased globally following US reclassification to Schedule I in 1984; all current methaqualone is clandestinely produced.[39]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Schedule II from 1973; reclassified Schedule I in 1984. No accepted medical use.[3][39] |
| United Kingdom | Class B (Misuse of Drugs Act 1971) | Withdrawn from clinical market in early 1980s following documented addiction and lethal overdoses.[2] |
| Canada | Schedule III (CDSA) | Controlled; no longer manufactured or clinically available. |
| Australia | Schedule 9 (Prohibited Substance) | Highest restriction category; no licensed manufacture, supply, or use. |
| European Union | Generally prohibited (varies by member state) | Restricted or prohibited in all member states. |
| South Africa | Illegal | Prohibited despite widespread illicit availability; Mandrax remains one of the most commonly seized illicit drugs.[5] |
| United Nations | Schedule II (Convention on Psychotropic Substances) | Initially placed in Schedule I; moved to Schedule II in 1979.[3] |
Analog act considerations
In the United States, novel quinazolinone analogs such as SL-164 may fall under the Federal Analogue Act if marketed for human consumption, though standard drug screening panels may not detect these analogs.[19]
references
- [1] ^abcdefghHammer H, Bader BM, Ehnert C, Bundgaard C, Bunch L, Hoestgaard-Jensen K, Schroeder OH, Bastlund JF, Gramowski-Voss A, Jensen AA (2015) A Multifaceted GABAA Receptor Modulator: Functional Properties and Mechanism of Action of the Sedative-Hypnotic and Recreational Drug Methaqualone (Quaalude) — Molecular Pharmacology doi:10.1124/mol.115.099291
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- [5] ^abcParry CD, Bhana A, Pluddemann A, Myers B, Siegfried N, Morojele NK, Flisher AJ, Kozel NJ (2002) The South African Community Epidemiology Network on Drug Use (SACENDU): description, findings (1997-99) and policy implications — Addiction PMID:12144599
- [6] ^abcHicks TP, Kaneko T, Oka JI (1990) Receptive-field size of S1 cortical neurones is altered by methaqualone via a GABA mechanism — Canadian Journal of Neurological Sciences PMID:2311013