Erowid References Database
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Holbrook LA.
“Transient Decrease in Brain Protein Synthesis after in vivo Administration of a Psychotropic Drug: Mechanism and Developmental Effects”.
Dissertation Abstr.Intern,B. 1979;39(7):3106.
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Abstract
Effects of i.v. LSD on translational apparatus of rabbit brain were studied. Polysomes in all regions of rabbit brain were affected: disaggregation was transient, being maximal 30-60 min after LSD injection and returning to control levels by 4 hr well after behavioral signs of hyperactivity had receded. No effect on kidney or spleen polysomes was found in animals, indicating brain specificity. Degree of polysome disaggregation increased with dosage over the range 10-100 mcg/kg. Over this same range, a consistent cortical arousal pattern was determined by EEG measures, indicating altered neuronal activity might be an element in this effect on macromolecular metabolism. At constant dosage of 50 mcg/kg, there was an increased degree of polysome shift with advancing postnatal age. There was essentially no effect on 3-wk-old animals with twice the percent shift in adults compared to 6k-old rabbits. Fetal polysomes were disaggregated in liver, kidney and brain, implying that a general physiological change acted on the fetus non-apecifically likely through alterations in maternal circulatory factor(s) such as amino acid levels. Fetal response led to experiments testing differences in holding cages or handling after LSD, both of which revealed potentiation of polysome disaggregation. Intraventricular injection of radioactive amino acids via implanted cannulas demonstrated a measurable decrease in protein synthesis during the 30-60 min of maximal polysome disaggregation. Protein specific activity was decreased in a range of cytoplasmic soluble and subfractionated membrane proteins after LSD. A particular membrane protein separated on slab gels from the synaptosome fraction was more hightly labeled during drug reatment than in controls. Salt dissociation and tRNA content of the increased monosome pool after LSD revealed that these were free ribosomes arising by run-off from the mRNA. A range of pharmacological agents administered prior to LSD indicated that serotonergic, dopaminergic and adrenergic transmitter receptors were involved in the process leading to polysome disaggregation. Neuronal activity also seemed to be a requirement, as disaggregation was blocked by general anesthetics, alcohol and pentobarbital.
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