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BRAIN RIBOSOMES IN INTRACRANIAL HYPERTENSION 1
Author(s) -
Wasterlain C. G.
Publication year - 1974
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1974.tb06942.x
Subject(s) - polysome , ribosome , in vivo , protein biosynthesis , perfusion , cerebrospinal fluid , messenger rna , monomer , intracranial pressure , cerebral perfusion pressure , chemistry , endocrinology , medicine , rna , biology , biochemistry , anesthesia , microbiology and biotechnology , organic chemistry , gene , polymer
— Increased intracranial pressure was produced by perfusion of cerebrospinal fluid (CSF) at various pressures into the lateral ventricles of adult Sprague‐Dawley rats with bilateral chronic intraventricular cannulas. When CSF perfusion was carried out at pressures of 150, 300 or 600 mm of water, brain polysomal profiles were similar to controls. Rats perfused under a pressure of 1500 mm water for 30 min were comatose, had slow electroencephalograms and showed a fall in brain polysomes from 66 to 24 per cent of the total ribosomes ( P < 0.01) while ribosomal monomers and dimers increased. These monomers and dimers were completely and reversibly dissociated into subunits in 500 niM KC1 buffers, unless prefixed in formaldehyde. [ 3 H]leucine incorporation into brain ribosomes in vivo was decreased by severe intracranial hypertension. In cell‐free systems in vitro , pathological ribosomes were less active in protein synthesis than controls ( P < 0.01) but were at least as readily stimulated by poly U. After intracranial pressure was returned to normal, there was a progressive reassociation of ribosomes into polysomes, even in the presence of Actinomycin D. These findings suggest that during severe intracranial hypertension cerebral protein synthesis is inhibited, perhaps through reversible inactivation of the translation of messenger RNA.