Gabapentin - PsychonautWiki


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Fatal overdose may occur when gabapentinoids are combined with other depressants such as opiates, benzodiazepines, barbiturates, thienodiazepines, alcohol or other GABAergic substances.[1]

It is strongly discouraged to combine these substances, particularly in common to heavy doses.

Summary sheet: Gabapentin
Chemical Nomenclature
Common names Gabapentin, Neurontin, Gabarone, Gralise
Substitutive name Gabapentin
Systematic name 1-(Aminomethyl)cyclohexaneacetic acid
Class Membership
Psychoactive class Depressant
Chemical class Gabapentinoid
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Bioavailability 27% - 60%[2]
Threshold 200 mg
Light 200 - 600 mg
Common 600 - 900 mg
Strong 900 - 1200 mg
Heavy 1200 mg +
Total 5 - 8 hours
Onset 30 - 90 minutes

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.


Gabapentin (also known as Neurontin) is a depressant substance of the gabapentinoid class. It is a structural analog of the neurotransmitter GABA and acts by inhibiting certain calcium channels in the brain namely α2δ subunit-containing voltage-dependent calcium channels (VGCCs).[3]

Gabapentin was originally developed to treat epilepsy and is currently FDA approved to treat postherpetic neuralgia in adults and as an adjunctive therapy in the treatment of partial onset seizures. It is often prescribed off-label for restless leg syndrome, social anxiety disorder, panic disorder, and generalized anxiety disorder.[4][5][6] However Gabapentin's efficacy in the treatment of anxiety disorders is unclear as the evidence is "somewhat mixed".[7][8][9][10] It is recommended as a first line agent for the treatment of neuropathic pain arising from diabetic neuropathy, post-herpetic neuralgia, and central neuropathic pain.[11]Subjective effects include mild to moderate anxiety suppression, pain relief, and muscle relaxation. Its analgesic and anxiolytic effects provide gabapentin with some recreational potential in a manner that can be compared to a mild benzodiazepine. However, these recreational effects diminish very quickly with repeated usage and are most commonly reported by those who do not have a tolerance to this compound.

Gabapentin should be taken with food as fasting will lead to less gabapentin exposure. The fat content of the food does not matter, though. [12]

Gabapentin is considered to have low abuse potential compared to most recreational depressants. However, chronic use can lead to physical dependence. Additionally, there is a risk of lethal overdose when it is combined with other depressants (a relatively common practice considering its weak effects). As a result, it is highly advised to use harm reduction practices if using this substance.


Gabapentin is a 3,3-disubstituted derivative of GABA. Therefore, it is a GABA analogue, as well as a γ-amino acid.[13] Specifically, it is a derivative of GABA with a pentyl disubstitution at 3 position, hence, the name - gabapentin, in such a way as to form a six-membered ring. After formation of the ring, the amine and carboxylic groups are not in the same relative positions as they are in the GABA:.[14] they are more conformationally constrained.[15]

Gabapentin, or 1-(aminomethyl)cyclohexylacetic acid, is an analogue of the neurotransmitter GABA. It contains a cyclohexane ring bound to a methylamino chain CH3NH2. At the same location, R1, the cyclohexane ring is also substituted with an acetic acid group. Gabapentin is structurally analogous to GABA. GABA contains an amino group bound to the terminal carbon of a butanoic acid chain. The structure of gabapentin contains the secondary carbon R3 of the butanoic acid chain in GABA incorporated into an attached cyclohexane ring, converting it into a tertiary carbon while still maintaining the chain.


Gabapentin modulates the action of glutamate decarboxylase (GAD) and branched-chain aminotransferase (BCAT), two enzymes involved in GABA biosynthesis. In human and rat studies, gabapentin was found to increase GABA biosynthesis, and to increase non-synaptic GABA neurotransmission in vitro.[16] As the GABA system is the most prolific inhibitory receptor set within the brain, its increase in biosynthesis results in the sedating and anxiolytic (or calming effects) of gabapentin on the nervous system.

Another study[17] based on magnetic resonance imaging done at 7 Tesla confirms that Gabapentin appears to increase cerebral GABA concentrations acutely, in vivo, by up to 79% from baseline.

Gabapentin, as a gabapentinoid, has also been shown to bind to the α2δ-1 subunit of Voltage-Gated Calcium Channels to act as a VGCC blocker, which contributes to its inhibitory, analgesic, and anxiolytic effects.[18] It is uncertain exactly how this method of action contributes to gabapentin's psychoactive effects.

The bioavailability of gabapentin is relatively low and is inversely proportional to the dose (i.e. higher doses have lower bioavailability than lower doses). The bioavailability of gabapentin is approximately 60%, 47%, 34%, 33%, and 27% following 900, 1200, 2400, 3600, and 4800 mg/day, given in divided doses of one pill per every 8 hours.[19] Gabapentin is highly lipophilic, making unsaturated fats such as vegetable oil and olive oil significantly boost the total amount of absorption. This means that eating a high fat meal substantially increases gabapentin's bioavailability, due to the fact that unsaturated fats bind to gabapentin to allow for absorption, and that meals slow down and thus increase gabapentin absorption by decreasing gabapentin transporter saturation.[20]

Gabapentin transporter saturation occurs when large enough doses of gabapentin are consumed in a short enough period of time to result in the body being unable to absorb any more gabapentin, causing a significant reduction in bioavailability, which largely accounts for the drop in bioavailability seen with increasing doses.

Gabapentin is a potent activator of voltage-gated potassium channels KCNQ3 and KCNQ5, even at low nanomolar concentrations. However, this activation is unlikely to be the dominant mechanism of gabapentin's therapeutic effects.[21]

Subjective effects

The decreasing bioavailability of gabapentin can be lessened by taking lower doses more often instead of higher doses less frequently. As a general rule, using any more than 250-300 mg of gabapentin every 30-45 minutes will result in wasting a significant portion of the total dose of gabapentin, although this number varies depending on the individual. Alkaline environments inhibit the absorption of gabapentin, so lowering the pH of one's stomach using acidic substances (such as soft drinks) will boost bioavailability as well. It is generally not recommended to take antacids 2 hours before or after taking gabapentin, because although not dangerous, it will severely lower the total absorption of gabapentin.[22]

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), a research literature based on collected anecdotal reports and the personal experiences of PsychonautWiki contributors. As a result, they should be regarded with a healthy degree of skepticism. It is worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce a full spectrum of effects. Likewise, adverse effects become much more likely with higher doses and may include addiction, serious injury, or death ☠.

Physical effects

Cognitive effects

Visual effects

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:

Toxicity and harm potential


This toxicity and harm potential section is a stub.

As a result, it may contain incomplete or even dangerously wrong information. You can help by expanding upon or correcting it.
Note: Always conduct independent research and use harm reduction practices if using this substance.

This document, provided with prescription gabapentin, contains detailed information regarding its toxicity and harm potential.

GABApentin has a low toxicity relative to dose. The most common side effects of gabapentin in adult patients include dizziness, fatigue, drowsiness, weight gain, and peripheral edema (swelling of extremities).[24] Gabapentin may also produce sexual dysfunction in some patients whose symptoms of which may include loss of libido, inability to reach orgasm, and erectile dysfunction.[25][26] Gabapentin should be used carefully in patients with renal impairment due to possible accumulation and toxicity.[27]

It is strongly recommended that one use harm reduction practices when using this drug.


In 2009, the U.S. Food and Drug Administration issued a warning of an increased risk of depression and suicidal thoughts and behaviors in patients taking gabapentin (along with other anticonvulsant drugs),[28] modifying the packaging insert to reflect this. A 2010 meta-analysis confirmed the increased risk of suicide associated with gabapentin use.[29]

Lethal dosage

People who accidentally or intentionally overdose may experience drowsiness, sedation, blurred vision, slurred speech, somnolence and possibly death (if a very high amount was taken and particularly if combined with alcohol). Serum gabapentin concentrations may be measured to confirm diagnosis.[30]

Dependence and abuse potential

Gabapentin is not considered psychologically addictive. However, it is possible to develop a physical dependence on the drug. In fact, people can experience withdrawal symptoms for up to 45 days after they stop taking gabapentin. Although gabapentin does give some people a euphoric “high” which can cause abuse, gabapentin abusers do not present with the kind of compulsive, drug-seeking behavior or strong cravings associated with other more common depressants such as opioids, alcohol or benzodiazepines.

Tolerance will develop to the anxiolytic effects with prolonged continuous usage. After cessation, the tolerance returns to baseline in 7-14 days. Withdrawal symptoms or rebound symptoms may occur after ceasing usage abruptly following a few weeks or longer of steady dosing and may necessitate a gradual dose reduction.

Dangerous interactions

  • Opioids - Combining opioids with gabapentin can cause death from respiratory failure.
  • Depressants (GABAergic) - Gabapentin significantly potentiates the effects of alcohol, benzodiazepines and other GABAergics which may lead to blackouts, and dangerous behaviour.

Legal status


This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

Gabapentin is a prescription-only medicine and can only be prescribed following a consultation with a doctor.[citation needed]

  • Germany: Gabapentin is a prescription medicine, according to Anlage 1 AMVV.[31]
  • Switzerland: Gabapentin is listed as a "Abgabekategorie B" pharmaceutical, which requires a prescription.[citation needed]
  • United States: Gabapentin is not a scheduled substance but may only be sold with prescription.[32]
    • Kentucky: Gabapentin became a Schedule 5 controlled substance in March 2017.[citation needed]

See also

External links


  1. Risks of Combining Depressants (Tripsit) |
  2. "Gabapentin dosing, indications, interactions, adverse effects, and more". |
  3. Calandre, Elena P.; Rico-Villademoros, Fernando; Slim, Mahmoud (2016). "Alpha2delta ligands, gabapentin, pregabalin and mirogabalin: a review of their clinical pharmacology and therapeutic use". Expert Review of Neurotherapeutics. 16 (11): 1263–1277. doi:10.1080/14737175.2016.1202764. ISSN 1473-7175. 
  4. Manual of Clinical Psychopharmacology |
  5. Successful Psychopharmacology: Evidence-Based Treatment Solutions for Achieving Remission |
  7. [1] The role of anticonvulsants in anxiety disorders: a critical review of the evidence.
  8. [2] Gabapentin Use in a Managed Medicaid Population
  9. [3] Promotion of Gabapentin
  10. Restless legs syndrome: clinical presentation diagnosis and treatment |
  11. EFNS guidelines on the pharmacological treatment of neuropathic pain: 2010 revision ( / NCBI) |
  12. [4] The effect of food with varying fat content on the clinical pharmacokinetics of gabapentin after oral administration of gabapentin enacarbil.
  13. Wyllie E, Cascino GD, Gidal BE, Goodkin HP (17 February 2012). Wyllie's Treatment of Epilepsy: Principles and Practice. Lippincott Williams & Wilkins. p. 423. ISBN 978-1-4511-5348-4.
  14. Sneader, Walter (2005). Drug Discovery: A History. John Wiley & Sons. pp. 219–220. ISBN 978-0-470-01552-0.
  15. Levandovskiy IA, Sharapa DI, Shamota TV, Rodionov VN, Shubina TE (February 2011). "Conformationally restricted GABA analogs: from rigid carbocycles to cage hydrocarbons". Future Medicinal Chemistry. 3 (2): 223–41. doi:10.4155/fmc.10.287. PMID 21428817.
  16. Mechanisms of action of gabapentin ( / NCBI) |
  17. The Impact of Gabapentin Administration on Brain GABA and Glutamate Concentrations: A 7T 1H-MRS Study ( / NCBI) |
  18. The mechanisms of action of gabapentin and pregabalin. ( / NCBI) |
  19. Neurontin Clinical Pharmacology Biopharmaceutics Review |
  20. Gabapentin datasheet |
  21. Manville RW, Abbott GW (October 2018). "Gabapentin Is a Potent Activator of KCNQ3 and KCNQ5 Potassium Channels". Mol Pharmacol. 94 (4): 1155–1163. doi:10.1124/mol.118.112953. PMC 6108572. PMID 30021858.
  23. Anticonvulsant medications and the risk of suicide, attempted suicide, or violent death. |
  30. R.C. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 677–8. ISBN 978-0-9626523-7-0.
  32. Peckham, A. M., Ananickal, M. J., & Sclar, D. A. (2018). Gabapentin use, abuse, and the US opioid epidemic: the case for reclassification as a controlled substance and the need for pharmacovigilance. Risk management and healthcare policy, 11, 109.