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A diagrammatic comparison of the structures of glutamate and various popular dissociatives.

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.[1]

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[2] and/or opioid[3] systems and are capable of inducing euphoria.

Mechanism of action

Further information: NMDA receptor antagonist

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.

Pharmacological classes

Subjective effects


Visual effects

See also

External links




  1. 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
  2. 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
  3. 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