LSD :: Hallucinogens Drugs Essays

lysergic acid diethylamide Lysergic dot Diethyl amide (lysergic acid diethylamide) has been implicated in a manakin of studies to determine its potential for order on certain neural activities. To date, little that nookie be certain as concrete fact has been found, though a number of theories with substantial support exist. Although dopamine, epinephrine, and norepinephrine may be implicated in whatsoever lysergic acid diethylamide studies, serotonin seems to be the main focus of scientific query with respect to lysergic acid diethylamide. Leicht (1996), postulates four theories concerning serotonin (5-HT) pre- and post-synaptic transmitter sites and the potential for LSD to affect these sites, in particular. All of these theories point to the synaptic neuronal dendrites and end point justtons as the main suspects with regard to LSD and its particular target field of operation on the neurons themselves. After considerable dialogue which analyses studies by Aghajanian and colleagues, Leicht came to the conclusion that the try out points toward certain types of activities on particular pre- and post-synaptic serotonergic neurons. The theories ar as follows1 LSD Pre-synaptically inhibits 5-HT neurons. 2 LSD Post-synaptically antagonizes 5-HT2 receptors.3 LSD Post-synaptically partially agonizes 5-HT receptors.4 LSD Post-synaptically agonizes 5-HT receptors. Neural clusters in the Raphe Nuclei, which spread out from there, mainly into the frontage and prefrontal cortices have been place as serotonergic. They are also auto-reactive, and LSD appears to inhibit the spontaneous firing of the neurons at that site, when the drug is remainsically administrated. 5-HT2 receptors have been identified as pH dependent, while LSD molecules have been identified as pH independent. 5-HT2 receptors are connected to a second messenger system (phosphatidyloniitol, or PI). PI turnover has been found to be affected by 5-HT2 in an antagonistic fashion , but is stimulated by 5-HT. LSD, in micrometric doses, can inhibit 1000 times that amount of 5-HT, which supports theory 2, as easily as supporting, partially, theory 3 when LSD is administered in a variety of doses, it apparently acts as a partial agonist. Though LSD and 5-HT are highly compatible, 5-HT is more effective at the serotonin receptor site, but LSD can compete with it at the 5-HT2 site. The conclusion is, since 5-HT is a more potent agonist than LSD, the effects of LSD would appear antagonistic. Finally, for theory 4, Leicht cites Dr. Glennons explanation of LSDs relationship with post-synaptic 5-HT receptors.