Mushy Mind – The real effects of Psilocybin

The real effects of Psilocybin

Written by Natty Dread – The U.S. government has determined psilocybin as having no medicinal value’—and everyone knows you can trust the U.S government.

Psilocybin is one of the list of chemicals present in many mushrooms. It is also one of my favorites. Expand your mind maaaaaan – Well new research shows that psilocybin may do just that.

Admittedly researchers were injecting directly into specific sites in the brains of mice, not sitting around a Pink Floyd record with a psychedelic brew in hand. But from what I understand the mice were smarter afterwards.

However if you’ve ever spoken to a group of headbangers who sat around a Pink Floyd record with a psychedelic brew in hand, they would probably tell you that they were smarter afterwards.

Researcher, Dr. Juan R. Sanchez-Ramos, tested the effects of psilocybin by training mice to fear an electric shock when they heard a noise associated with the shock. Then, by giving them psilocybin, the mice were able to stop reacting to the noise-trigger much faster than those mice not treated.

“The proposition that psilocybin impacts cognition and stimulates hippocampal neurogenesis is based on extensive evidence that serotonin (5-hydroxytryptamine or 5-HT) acting on specific 5-HT receptor sub-types (most likely the 5-HT2A receptor) is involved in the regulation of neurogenesis in hippocampus,” says Dr. Sanchez-Ramos according to NaturalNews. “The in vitro and in vivo animal data is compelling enough to explore whether psilocybin will enhance neurogenesis and result in measurable improvements in learning.”

Exp Brain Res. 2013 Aug;228(4):481-91. doi: 10.1007/s00221-013-3579-0. Epub 2013 Jun 2
Learn more: http://www.naturalnews.com

The hippocampus is part of the brain responsible for learning as well as converting short-term memory to long-term memory.

It basically comes down to the possibility that it may be able to help improve cognition and even to actually help repair damaged brain cells as well as treating depression and post-traumatic stress disorders as a side effect.

(People suffering from depression apparently have an overactive prefrontal cortex – psilocybin literally switches off the anterior cingulate cortex, allowing depressed individuals to experience relief)

Pretty fucking cool huh?

One thing I took from that (and my own private psilocybin research) which may have passed the scientists by was that the treated mice stopped reacting to the conditioned triggers quicker. – A trait which I have also observed in human psilocybin guinea pigs. People mistake the blank eyed stares of the terminally smashed as symptoms of drug psychosis, when maybe they are simply failing to react to conditioned social triggers? Just like the mice? Perhaps they’re too busy using their stimulated hippocampal neurogenesis to think about higher things? Like ewoks.

But then again I’m not a scientist. I’m a headbanger with more than on Pink Floyd album in my collection. So maybe you should just watch this vid from Dr. Juan R. Sanchez-Ramos (and the guys who did the research) and form your own opinions?

And if you’re interested the article detailing the experiment-

Effects of psilocybin on hippocampal neurogene… [Exp Brain Res. 2013] – PubMed – NCBI

Effects of psilocybin on hippocampal neurogenesis and extinction of trace fear conditioning.

Catlow BJ1, Song S, Paredes DA, Kirstein CL, Sanchez-Ramos J.

Author information

Abstract
Drugs that modulate serotonin (5-HT) synaptic concentrations impact neurogenesis and hippocampal (HPC)-dependent learning. The primary objective is to determine the extent to which psilocybin (PSOP) modulates neurogenesis and thereby affects acquisition and extinction of HPC-dependent trace fear conditioning. PSOP, the 5-HT2A agonist 25I-NBMeO and the 5-HT2A/C antagonist ketanserin were administered via an acute intraperitoneal injection to mice. Trace fear conditioning was measured as the amount of time spent immobile in the presence of the conditioned stimulus (CS, auditory tone), trace (silent interval) and post-trace interval over 10 trials. Extinction was determined by the number of trials required to resume mobility during CS, trace and post-trace when the shock was not delivered. Neurogenesis was determined by unbiased counts of cells in the dentate gyrus of the HPC birth-dated with BrdU co-expressing a neuronal marker. Mice treated with a range of doses of PSOP acquired a robust conditioned fear response. Mice injected with low doses of PSOP extinguished cued fear conditioning significantly more rapidly than high-dose PSOP or saline-treated mice. Injection of PSOP, 25I-NBMeO or ketanserin resulted in significant dose-dependent decreases in number of newborn neurons in hippocampus. At the low doses of PSOP that enhanced extinction, neurogenesis was not decreased, but rather tended toward an increase. Extinction of “fear conditioning” may be mediated by actions of the drugs at sites other than hippocampus such as the amygdala, which is known to mediate the perception