Dissociatives (also referred to as dissociative anesthetics) are a class of hallucinogen. Members of this class are characterized by distorted sensory perceptions and feelings of disconnection or detachment from the environment and self. The phenomenology is often described in terms of reducing or blocking signals to the conscious mind from other parts of the central nervous system.
Many dissociatives have general depressant effects and can produce sedation, respiratory depression, analgesia, anesthesia, and ataxia, as well as cognitive and memory impairment and amnesia. Some dissociatives affect the dopamine and/or opioid systems and are capable of inducing euphoria.
- 1 Mechanism of action
- 2 Pharmacological classes
- 3 Subjective effects
- 4 See also
- 5 External links
- 6 Literature
- 7 References
Mechanism of action
NMDA receptors within the brain exist to allow for the transfer of electrical signals between neurons in the brain and in the spinal column. For electrical signals to pass, the NMDA receptor must be open. To remain open, the neurotransmitters known as glutamate and glycine must bind to the NMDA receptor. An NMDA receptor that has glycine and glutamate bound to it and has an open ion channel is called "activated."
Dissociatives are classed as NMDA receptor antagonists. This means they bind to the receptor, but do not activate it and block other neurotransmitters from doing so. The result is a dose dependent decrease in the passing of electrical signals across the brain and an overall disconnection of neurons. This leads onto states of disconnection between conscious parts of the brain and its sensory organs as well as out-of-body experiences and accompanying hallucinations.
Disclaimer: The effects listed below are taken from the subjective effect index, which is based on anecdotal reports and the personal experiences of PsychonautWiki contributors. As a result, they should be treated with a healthy degree of skepticism. It is worth noting that these effects will rarely (if ever) occur all at once, although higher doses will increase the chances of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.
In comparison to other classes of hallucinogen, this effect is significantly less complex and intricate with a limited range of effects. It does not extend beyond level 4 and is variable within most of its variations but is exclusively simplistic in complexity, unstructured in organization, dimly lit in lighting, slow in movement and immersive in depth.
- Perspective alterations
- Autonomous entities
- Scenarios and plots
- Settings, sceneries, and landscapes
- Shadow people
It can be comprehensively described through its variations as delirious in believability, autonomous in controllability and solid in appearance.
The most common theme for this effect to follow is one of experiencing and talking to friends around oneself when they are not actually present.hallucinogen, this effect can occur at heavy dosages but is considerably less common than the same effect found within psychedelics and deliriants.
It can be comprehensively described through its variations as delirious in believability, fixed in style, equal in new experiences and memory replays in content, autonomous in controllability and solid in appearance.
- Conceptual thinking
- Cognitive euphoria
- Déjà vu
- Dream potentiation
- Increased music appreciation
- Analysis suppression
- Memory suppression
- Personal bias suppression
- Autonomous voice communication
- Thought connectivity
- Thought deceleration
- Thought loops
- Time distortion
- Unity and interconnectedness
- Morris, H., & Wallach, J. (2014). From PCP to MXE: A comprehensive review of the non-medical use of dissociative drugs. Drug Testing and Analysis, 6(7–8), 614–632. https://doi.org/10.1002/dta.1620
- PCP-induced alterations in cerebral glucose utilization in rat brain: blockade by metaphit, a PCP-receptor-acylating agent.| http://www.ncbi.nlm.nih.gov/pubmed/2850626
- Giannini, A. James; Nageotte, Catherine; Loiselle, Robert H.; Malone, Donald A.; Price, William A. (1984). "Comparison of Chlorpromazine, Haloperidol and Pimozide in the Treatment of Phencyclidine Psychosis: Da-2 Receptor Specificity". Clinical Toxicology 22 (6): 573–9. (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/6725621
- Giannini, A. James; Underwood, Ned A.; Condon, Maggie (2000). "Acute Ketamine Intoxication Treated by Haloperidol". American Journal of Therapeutics 7 (6): 389–91. (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/11304647