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Effects of a single dose of psilocybin on behaviour, brain 5-HT2A receptor occupancy and gene expression in the pig

ABSTRACT: Effects of a single dose of psilocybin on behaviour, brain 5-HT2A receptor occupancy and gene expression in the pig

PROVIDER: PRJNA721958 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14238813_1.fastq.gz	Fastqsanger.gz
	SRR14238813_2.fastq.gz	Fastqsanger.gz
	SRR14238814_1.fastq.gz	Fastqsanger.gz
	SRR14238814_2.fastq.gz	Fastqsanger.gz
	SRR14238815_1.fastq.gz	Fastqsanger.gz

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Effects of a single dose of psilocybin on behaviour, brain 5-HT2A receptor occupancy and gene expression in the pig

Project description:mRNA sequencing of pig prefrontal cortex after treatment with one dose of psilocybin or placebo (saline).

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Project description:Psilocybin, and other serotonergic psychedelics, have re-emerged as therapeutics for neuropsychiatric disorders, including addiction. Psilocybin induces long-lasting effects on behavior, likely due to its profound ability to alter consciousness and augment neural connectivity and plasticity. Impaired synaptic plasticity in obesity contributes to ‘addictive-like’ behaviors, including heightened motivation for palatable food, and excessive food seeking and consumption. Here, we evaluate the effects of psilocybin on feeding behavior, energy metabolism and as a weight-lowering agent in mice. We demonstrate that a single dose of psilocybin substantially alters the prefrontal cortex transcriptome but has no acute or long-lasting effects on food intake or body weight in diet-induced obese mice or in genetic mouse models of obesity. Similarly, sub-chronic microdosing of psilocybin has no metabolic effects in obese mice and psilocybin does not augment glucagon-like peptide-1 (GLP-1) induced weight loss or enhance diet-induced weight loss. A single high dose of psilocybin reduces sucrose preference but fails to counter binge-like eating behavior. Although these preclinical data discourage clinical investigation, there may be nuances in the mode of action of psychedelic drugs that are difficult to capture in rodent models, and thus require human evaluation to uncover.

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Project description:Advanced clinical trials investigate the Psilocybe magic mushroom natural product psilocybin as a treatment against major depressive disorder. Currently, synthetic material is used to meet the demand for legitimate pharmaceutical purposes. Here, we report an in vitro approach to biocatalytically produce psilocybin on a solid-phase matrix charged with five covalently bound biosynthetic enzymes. These enzymes include three Psilocybe enzymes: IasA, an engineered L-tryptophan decarboxylase/aromatic aldehyde synthase, the 4-hydroxytryptamine kinase PsiK and the norbaeocystin methyltransferase PsiM, along with Escherichia coli nucleosidase MtnN and adenine deaminase Ade. In a proof-of-principle experiment, this enzyme-charged resin allowed for quantitative turnover of 4-hydroxy-L-tryptophan into psilocybin. This facile process i) represents a sustainable approach with reusable enzymes, ii) circumvents the drawbacks of in vivo processes while harnessing the selectivity of enzymatic catalysis and iii) helps access an urgently needed drug candidate.

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gene expression analysis of the rat prefrontal cortex following psilocybin or ketanserin administration

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Psilocybin Elicits a Conserved Glucocorticoid-Responsive Gene Signature Across Five 5-HT2A Receptor-Rich Brain Regions in the Male Rat

Project description:psychedelics are a class of substances best known for their extraordinary mind-altering effects, psychoactive properties that give them both opportunities and risks towards people’s mental health. Based on evidence from clinical trials, psilocybin, a widely used psychedelic for research purposes, appears to produce long-lasting therapeutic effects with minimal physical side effects in patients with a range of mood and addictive disorders. However, as psilocybin profoundly impacts perception, emotion, cognition and the sense of self, it is difficult to use it in the same way that ordinary candidate compounds with therapeutic potential are tested in routine daily clinical trials. Preclinical experiments can therefore provide valuable insights into the molecular mechanisms underlying the reported clinical effectiveness of the compound. Several lines of evidence strongly suggest that psilocybin exerts its effects through 5-HT2A receptors located postsynaptically to serotonergic neurons, particularly concentrated in the frontal cortex, parts of the limbic system (i.e., amygdala and hippocampus), and striatum. In an attempt to improve our knowledge of regional patterns of gene expression in the brain induced by psilocybin, we have generated a global map of gene expression in selected regions of adult rat brain (medial prefrontal cortex, cingulate cortex, hippocampus, and striatum; both right and left sides) using 3prime-RNASeq technology. While our findings revealed a few differentially expressed genes (DEGs) to be present in two or more regions, others had a region-specific profile. Additionally, pathways normally activated by glucocorticoids were found to be enriched in all the examined brain regions following psilocybin treatment.

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