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it's been noticed that psilocyn can indirectly raise dopamine concentration withing the basal ganglia.

Almost 50% of oral psilocybin is absorbed by stomach and gut; from here is lead to liver, where it's converted in psilocin, pharmacologically active form, that can furtherly be glucoronated and escreted with urine or converted in other psilocinics metabolites.

In rats, the median lethal dose (LD50) when administered orally is 280 milligrams per kilogram (mg/kg), approximately one and a half times that of caffeine. When administered intravenously in rabbits, psilocybin's LD50 is approximately 12.5 mg/kg

traces of the compund can be detected in unine even after 7 days.

Clinical studies show that psilocin concentrations in the plasma of adults average about 8 µg/liter within 2 hours after ingestion of a single 15 mg oral psilocybin dose; psychological effects occur with a blood plasma concentration of 4–6 µg/liter. Psilocybin is about 100 times less potent than LSD on a weight per weight basis, and the physiological effects last about half as long.

Within 24 hours from administration 65% of the alucinogen is escreted by urine, while another 15-20% is excreted by bile and feces.

Monoamine oxidase inhibitors (MAOI) have been known to prolong and enhance the effects of psilocybin. Alcohol consumption may enhance the effects of psilocybin, because acetaldehyde, one of the primary breakdown metabolites of consumed alcohol, reacts with biogenic amines present in the body to produce MAOIs related to tetrahydroisoquinoline and β-carboline. Tobacco smokers can also experience more powerful effects with psilocybin, because tobacco smoke exposure decreases levels of MAO in the brain and peripheral organs.

This could lead to a lower usage o f glucose, but the same study admitted an increase glucose usage by the whole brain cell, meaning a differente use of this sugar while the drug is having effects.

use of MRI (functional magnetic resounance) showed that the decresed blood flow associate with decreasing in neural activity. A simple explanation for this unexpected situation could be the serotoning agonist action of psilocybin, action that seems to be focused more on 5-HT receptors than on 5-HT2A.

psilocibyn is able to act as a 5-HT agonist binding directly its receptors.

augmented glucose consumption in several brain regions; this lead to the conclusion that psilocybin is some way able to modify the physiological glucosal metabolic rate of our body

The strong inibition of the PCC is now thought to be most significant action of psilocybin on neural disaccoppiation

Psilocybin comprises approximately 1% of the weight of Psilocybe cubensis mushrooms, and so nearly 1.7 kilograms (3.7 lb) of dried mushrooms, or 17 kilograms (37 lb) of fresh mushrooms, would be required for a 60-kilogram (130 lb) person to reach the 280 mg/kg LD50 value.

psilocybin can cause anxiety and increased heart rate and BP which is very counter- productive for someone on metoprolol and micardis.

propose the possibility to use psilocybin as a palliative therapy for terminal illness like cancer but also as a real antidepressive active principle available for the family of the patient. The rational is foundable in the fact that we usually administer SSRI as antidepressive agents, so psilocibyn sholud be useful in this purpose for its selective agonist action on 5-HT2A receptors