What´s Lysergic Acid Diethylamide?

Lysergic acid diethylamide is a natural substance synthesized from the parasitic rye fungus, Claviceps purpurea2. Albert Hofmann, a natural products chemist at the Sandoz AG Pharmaceutical Company, synthesized it in 1938 while experimenting with pharmaceutical uses for ergot2,4. He intended for this series known as LSD-25 to be used as a circulatory and respiratory stimulant. However, after minimal testing LSD-25 aroused no special interest in the pharmacologists and physicians. Testing was then discontinued and not worked with until his curiosity struck him 5 years later. In 1943 he repeated the synthesis of LSD-25. In the final step of the synthesis Hoffman was interrupted during his work by unusual sensations. He described these symptoms

In previous experiments dosing of animals with very high doses of LSD led to autonomic changes of tachycardia, tachypnea ,mydriasis, hyperthermia, hypertonia, and hyperglycemia. These changes may be the result of an excitatory syndrome caused by central stimulation of the sympathetic system. LSD affects both the sympathetic as well as parasympathetic stimulation. Sympathetic stimulation in most subjects is shown by a pupillary dilation and light to moderate increases in heart rate and blood pressure. Parasympathetic stimulation is displayed by salivation, nausea, emesis, and flushing of the face. Most somatic effects ascribed to LSD are thought to be secondary effects caused by the psychological reaction to the drug2.
Tolerance in LSD use is rare. However, cases where a user might take repeated doses within the same 48-72 hours can lead to a tolerance. The repeated use of LSD over short periods of time will require the user to double or triple their doses to achieve the same effects, which can lead to psychological dependence. There is currently little evidence that LSD is physically addicting and does not produce any withdrawal tendencies. However, psychological dependence to LSD is likely. Although, it is purely mental and can be overcome through psychological

In a study performed by Gonzalez-Maeso, he compared 5-HT2A agonists with and without hallucinogenic activity in mice. He found that these types of agonists differ in regard to the G-protein activation induced. Using mice modified to genetically express 5-HT2A receptors only in the cortex, it was shown that these receptors were sufficient to produce hallucinogenic effects2. This was indicated by hallucinogen-specific head twitch response with identical firing rates of pyramidal neurons as without this manipulation5. This may imply that the hallucinogenic effects are mainly mediated by cortico-cortical neural