The effects of hyperthermia on polyribosomes and amino acid levels in infant rat brain

EFFECTS OF ACUTE HYPERTHERMIA ON POLYRIBOSOMES, IN VIVO PROTEIN SYNTHESIS AND ORNITHINE DECARBOXYLASE ACTIVITY IN THE NEONATAL RAT BRAIN

“…Because many disaggregating agents are neuroactive drugs with known effects on body temperature, and because it has been demonstrated that hyperthermia exerts a permissive effect on the polyribosome disaggregating actions of amphetamine (MOSKOWITZ et al, 1977), we have been investigating the actions of acute hyperthermia per se on brain polyribosome integrity and associated parameters. Acute hyperthermia was found to produce a profound but reversible disaggregation of brain polyribosomes and a concomitant large increase in brain free amino acid levels in the neonatal rat (MURDOCK et a/., 1978). The present report describes experiments which indicate that these actions of hyperthermia d o occur in cioo.…”

“…These effects on in uivo protein synthesis were reversible, as shown by the results of experiments in which hyperthermic rats were allowed to rccover for 2 h at 33°C. We have previously demonstrated that the disaggregation of brain polyribosomes and increase in brain free amino acid levels which take place during hyperthermia also are reversed by a 2 h recovery period (MURDOCK et al, 1978).…”

“…Control rats and rats recovering from hyperthermia were kept at 33°C. a temperature previously shown to maintain maximal aggregation of brain polyribosomes (MURDOCK et al, 1978). Control rats used in studying the effects of hyperthermia and recovery were kept apart from the mother for as long a period of timc as the experimental animals in order to equalize any biochemical effects of maternal deprivation (BUTLER ,& SCHANBERG, 1977).…”

Characterization of a Translational Inhibitor Isolated from Rabbit Brain Following Intravenous Administration of d‐Lysergic Acid Diethylamide

“…A wide variety of physical and chemical treatments has been shown to result in a perturbation of protein synthesis in the mammalian brain, as evidenced by a reduction in the incorporation of amino acid into brain proteins and a disaggregation of brain polysomes to monosomes (for review, see Brown et al, 1982). A lesion in the initiation process has been suggested to result following amino acid imbalances (Taub and Johnson, 1975;Hughes and Johnson, 1977), cerebral hypoxia (Morimoto et al, 19781, ischemia (Cooper et al, 1977), electroconvulsive shock (Metafora et al, 1977), epileptic seizures (Wasterlain, 1977;Fando et al, 1979), and hyperthermia (Murdock et al, 1978;Brown et al, 1982;Brown, 1985). Suggested mechanisms of inhibition include a shift in the availability of aminoacyl-tRNAs (Taub and Johnson, 1975), depletion of cell energy reserves (Wasterlain, 1977), and changes in pH (Morimoto et al, 1978).…”

Fever's Glass Ceiling

“…Thermal sensitivity of the brain, but not other vital organs, has been attributed to the unique susceptibility of its polyribosomes to thermal injury [20]. At 40°C-42°C, these polyribosomes begin to disaggregate; above 41°C, irreversible destruction of cerebral mitochondria occurs [21,22]. However, in most animals thermal death occurs well below temperatures causing coagulation of proteins or denaturation of enzymes [23].…”