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Effect of LSD-25 (lysergic acid — diethyl amide) on the Energetic Metabolism of the Brain of Rats

V. Máthé, G. Kassay

International Pharmacopsychiatry August 11, 2017 DOI: 10.1159/000467933 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Animal experiment Peer reviewed
Population White rats
Interventions LSD-25 chlorpromazine
Dose LSD-25 2 gamma per 100 g; chlorpromazine 0.30 mg per 100 g
Duration Twenty minutes after injection
Topics LSD
Key findings LSD-25 and chlorpromazine produced opposing metabolic changes in rat brain tissue, with LSD-25 effects interpreted as dissimilatory and chlorpromazine effects as assimilatory. The authors report partial antagonism between the two drugs on brain carbohydrate metabolism and discuss possible relevance to LSD psychosis.

Abstract

Authors investigated the effect of LSD-25, of chlorpromazine, and of a combination of both on three parts of the brain of white rats (I: cortex and white substance extending to the subcortex; II: subcortical ganglia and medulla oblongata; III: cerebellum) upon the level of total reducing substance, glycogen, lactic, and pyruvic acid, ATP, and anorganic P. Twenty minutes after injecting 2ɣ per 100 g of LSD-25, subcutaneously, in I the glycogen level increased significantly, that of total reducing substance significantly decreasing. In II: concentration of both metabolites showed significant decrease. In III: that of pyruvic acid decreased nearly significantly. The so-called ‘Whole Brain Value’ computed from the average of total reducing substance, and pyruvic acid contents as found in the three brain parts showed a significant decrease. Twenty minutes after injecting, subcutaneously, 0.30 mg per 100 g of chlorpromazine the content of total reducing substance increased significantly in II and III, the glycogen level increased nearly significantly in II where lactic acid showed a significant decrease while pyruvic acid concentration decreased significantly in all three parts. The ‘Whole Brain Value’ of the latter showed a significant decrease, total reducing substance and glycogen content increased nearly significantly. Twenty minutes after injecting, subcutaneously, 2ɣ per 100 g of LSD-25 and 0.30 mg per 100 g of chlorpromazine the ATP level in III decreased significantly, that of anorganic P showing a significant increase. The ‘Whole Brain Value’ of pyruvic acid decreased significantly, that of anorganic P increased, also significantly. Authors consider the metabolic change caused by LSD-25 to be of a dissimilatory type, that upon chlorpromazine of assimilatory type relating them to the excitatory phenomena of the central nervous system as caused by LSD-25, and the inhibitive phenomena as caused by chlorpromazine. They found a partial antagonism between the effect of both drugs upon the carbohydrate metabolism of the brain tissue. On the grounds of literary data they discuss to what degree their results might be utilized for explaining the biochemical basic processes of LSD psychosis.

Comparable studies

Other preclinical and animal studies on LSD, most cited first.

Study Year Design Participants
Transcriptome Fingerprints Distinguish Hallucinogenic and Nonhallucinogenic 5-Hydroxytryptamine 2A Receptor Agonist Effects in Mouse Somatosensory Cortex Human embryonic kidney 293 cells stably expressing 5-HT2ARs; wild-type and 5-HT2AR... 2003 Experimental study
Evidence for a central 5‐hydroxytryptamine receptor stimulation by lysergic acid diethylamide Rats 1968 Experimental study
Psychedelics, but Not Ketamine, Produce Persistent Antidepressant-like Effects in a Rodent Experimental System for the Study of Depression Rats 2020 Preclinical study
Lysergic acid diethylamide (LSD) promotes social behavior through mTORC1 in the excitatory neurotransmission Male mice 2021 Multidisciplinary experimental study with in vivo electrophysiology, optogenetics, behavioral paradigms, molecular biology, and conditional knockout mice
A non-hallucinogenic LSD analog with therapeutic potential for mood disorders. Mice and cultured rat cortical neurons 2023 Preclinical study

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