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A diagrammatic comparison of the structures of glutamate and various popular dissociatives.
Dissociatives refer to a class of hallucinogen which distort sensory perceptions (mainly of sight and sound) to produce feelings of disconnection, detachment, and dissociation from the environment and self. This is done by reducing or blocking signals to the conscious mind from other parts of the brain.[1]
Диссоциативы — refer to a class of hallucinogen which distort sensory perceptions (mainly of sight and sound) to produce feelings of disconnection, detachment, and dissociation from the environment and self. This is done by reducing or blocking signals to the conscious mind from other parts of the brain.[1]
Although many classes of psychoactive substances are capable of such action, dissociatives are unique in that they do so in such a way that they produce hallucinogenic effects, which generally include sensory deprivation, dissociation, hallucinations, and dream-like states or trances.[2] Some dissociatives, which are non-selective in action and affect the dopamine[3] and/or opioid[4] systems, may also be capable of inducing euphoria.
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.
Эффекты
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe 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.
In comparison to other classes of hallucinogen, this effect can occur at heavy dosages, but is extremely infrequent in comparison to the same effect found within deliriants.
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.
In comparison to other classes of 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.
↑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
