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

Millan, Noemi; Murdock, Larry L.; Bleier, Ruth; Siegel, Frank L.

doi:10.1111/j.1471-4159.1979.tb00353.x

Cited by 36 publications

(9 citation statements)

References 20 publications

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“…Two procedures that were intended to be controls for the intracerebral injection of actinomycin D, drilling burr holes without puncturing the dura, and an intracerebral injection of mannitol (vehicle for actinomycin D), also induced ODC activity (Table I), probably due to mechanical and thermal trauma associated with drilling into the skull and injection damage. Stimulation of brain ODC activity by intracerebral injections and hyperthermia is consistent with previous reports (Millan et al. 1979: Hietala, 1983).…”

Section: Resultssupporting

confidence: 92%

“…For example, noxious conditions that interrupt energy metabolism or other critical processes can impair protein synthesis and cause the rapid influx of calcium into the injured cell. Brain protein synthesis is inhibited by metabolic, chemical, and thermal injuries (Kleihues et al, 1975;Moskowitz et a]., 1977;Millan et al, 1979), and abnormal proteins are produced after injection of the amino acid analog L-canavanine (Waterlow et al, 1978). Recovery from disruption of the homeostatic balance between protein synthesis and degradation may require preferential production of ( I ) proteins with short half-lives, such as ODC, to compensate for their rapid loss (e.g., after ischemia; Kleihues et al, 1975), or (2) other proteins required for the recovery process.…”

Section: Odc and Brain Injurymentioning

confidence: 99%

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Induction of Brain Ornithine Decarboxylase During Recovery from Metabolic, Mechanical, Thermal, or Chemical Injury

Dienel

Cruz

1984

Journal of Neurochemistry

155

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Metabolic, mechanical, thermal, and chemical injury induced ornithine decarboxylase (ODC) activity in rat brain. A two- to sixfold increase in ODC activity was measured at 5-9 h after different modes of injury to the brain. During the early phase of recovery from transient ischemia, when average protein synthesis was less than 50% of control, ODC activity was increased nearly fivefold. The rise in activity could be blocked by anisomycin, or reduced by intracerebral injections of actinomycin D. Drilling burr holes into the skull, injection of the vehicle for actinomycin D, hyperthermia, and freezing lesions all caused increased ODC activity. Neurotoxic chemicals (ammonia, methionine sulfoximine, acrylamide, carbon tetrachloride, and anisomycin) also increased brain ODC activity, whereas other chemicals (mannitol and valine) did not. Treatments known to stimulate the synthesis of heat shock proteins (carotid occlusion, hyperthermia, Cd2+, canavanine, and ethanol) induced ODC activity in the liver, whereas only hyperthermia and ethanol caused significant increases in spleen ODC activity. All increases in ODC activity were blocked by difluoromethylornithine, an irreversible inhibitor of ODC. The cellular response to noxious or stressful stimuli includes the synthesis of a small number of proteins of unknown functions; ODC may be one of these "heat shock" or "trauma" proteins.

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Section: Resultssupporting

confidence: 92%

Section: Odc and Brain Injurymentioning

confidence: 99%

Induction of Brain Ornithine Decarboxylase During Recovery from Metabolic, Mechanical, Thermal, or Chemical Injury

Dienel

Cruz

1984

Journal of Neurochemistry

155

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“…Because the brain is more easily damaged by high temperatures than other bodily organs (Heikkila & Brown, 1979;Millan, Murdock, Bleier, & Siegel, 1979), a number of species have evolved physiological mechanisms that selectively cool the brain during exercise and during exposure to high air temperatures. For example, Crawford (1972) studied a lizard species (Sauromalus obesus) that, when panting, can maintain brain temperature nearly 3ЊC below an air temperature of 45ЊC.…”

Section: Selective Brain Cooling In Reptiles Birds and Mammalsmentioning

confidence: 99%

Thermoregulatory competence and behavioral expression in the young of altricial species?Revisited

1998

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The behavioral and physiological thermoregulatory capabilities of newborn and infant mammals have been studied for over half a century. Psychobiologists have noted that the infants of altricial species (e.g., rats) have physical and physiological limitations such that heat loss overwhelms heat production, thus forcing a reliance on behavioral thermoregulation for the maintenance of body temperature. Recent evidence, however, suggests that a modification of this view is justified. Specifically, throughout a range of moderately cold air temperatures, nonshivering thermogenesis by brown adipose tissue contributes significantly to the infant rat's behavioral and physiological adaptations to cold challenge. Given the prominent use of altricial species for the study of infant behavior, increased understanding of the infant's physiological responses to cold and the effect of thermal factors on behavior is warranted. © 1998 John Wiley & Sons, Inc. Dev Psychobiol 33: 107–123, 1998

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“…Since the 75K and 95K proteins are induced under similar conditions in a number of different cultured cell lines, it has been suggested that these proteins may be important for cell survival under stressful conditions such as temperature elevation and energy deprivation (Kelley and Schlesinger, 1978). Brain functions are particularly sensitive to such stresses (Ritter and Ritter, 1977;Millan et al, 1979). In addition to providing information on the effect of the psychotropic drug LSD on protein synthesis in the mammalian brain, our present studies demonstrate the sensitivity of the translational apparatus in the brain to hyperthermia.…”

Section: Discussionmentioning

confidence: 99%

Effect of Intravenous Administration of d‐Lysergic Acid Diethylamide on Subsequent Protein Synthesis in a Cell‐Free System Derived from Brain

Cosgrove

Clark

Brown

1981

Journal of Neurochemistry

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An initiating cell-free protein synthesis system derived from brain was utilized to demonstrate that the intravenous injection of d-lysergic acid diethylamide (LSD) to rabbits induced a transient inhibition of translation following a brief stimulatory period. Subfractionation of the brain cell-free system into postribosomal supernatant (PRS) and microsome fractions demonstrated that LSD in vivo induced alterations in both of these fractions. In addition to the overall inhibition of translation in the cell-free system, differential effects were noted, i.e., greater than average relative decreases in in vitro labeling of certain brain proteins and relative increases in others. The brain proteins of molecular weights 75K and 95K, which were increased in relative labeling under conditions of LSD-induced hyperthermia, are similar in molecular weight to two of the major "heat shock" proteins reported in tissue culture systems. Injection of LSD to rabbits at 4 degrees C prevented LSD-induced hyperthermia but behavioral effects of the drug were still apparent. The overall decrease in cell-free translation was still observed but the differential labeling effects were not. LSD appeared to influence cell-free translation in the brain at two dissociable levels: (a) an overall decrease in translation that was observed even in the absence of LSD-induced hyperthermia and (b) differential labeling effects on particular proteins that were dependent on LSD-induced hyperthermia.

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

Cited by 36 publications

References 20 publications

Induction of Brain Ornithine Decarboxylase During Recovery from Metabolic, Mechanical, Thermal, or Chemical Injury

Induction of Brain Ornithine Decarboxylase During Recovery from Metabolic, Mechanical, Thermal, or Chemical Injury

Thermoregulatory competence and behavioral expression in the young of altricial species?Revisited

Effect of Intravenous Administration of d‐Lysergic Acid Diethylamide on Subsequent Protein Synthesis in a Cell‐Free System Derived from Brain

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