Fate of mRNA following disaggregation of brain polysomes after administration of (+)-lysergic acid diethylamide in vivo

Injecting (+)-lysergic acid diethylamide into young rabbits caused a temporary breakdown of brain polysomes into monosomes, indicating inhibited protein synthesis. The messenger RNA (mRNA) remained intact and was not degraded or released; instead, it accumulated on monosomes. The mRNA coding for a brain-specific protein, S100, was preserved. The formation of a blocked monosome complex containing intact mRNA and ribosomal subunits but lacking nascent peptide chains suggests that (+)-lysergic acid diethylamide disrupts brain protein synthesis at a specific step during late initiation or early elongation.

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Abstract

Intravenous injection of (+)-lysergic acid diethylamide into young rabbits induced a transient brain-specific disaggregation of polysomes to monosomes. Investigation of the fate of mRNA revealed that brain poly(A+)mRNA was conserved. In particular, mRNA coding for brain-specific S100 protein was not degraded, nor was it released into free ribonucleoprotein particles. Following the (+)-lysergic acid diethylamide-induced disaggregation of polysomes, mRNA shifted from polysomes and accumulated on monosomes. Formation of a blocked monosome complex, which contained intact mRNA and 40-S plus 60-S ribosomal subunits but lacked nascent peptide chains, suggested that (+)-lysergic acid diethylamide inhibited brain protein synthesis at a specific stage of late initiation or early elongation.