Age-dependent changes in brain protein synthesis in the rat

Fando, Juan L.; Salinas, Matilde; Wasterlain, Claude G.

doi:10.1007/bf00964226

Cited by 54 publications

(16 citation statements)

References 46 publications

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“…Prior to this time, the experimental methods did not consider specific activity of the precursor pool (reviewed by Richardson and Birchenall-Sparks, 1983), which resulted in highly variable outcomes across studies. Using improved methodology, several groups found that levels of brain protein synthesis increase during development in the rodent, reaching maximum levels sometime during the first 6 months of age, and then decline thereafter (Dwyer et al, 1980; Ekstrom et al, 1980; Fando et al, 1980; Ingvar et al, 1985; Smith et al, 1995; but see Filion and Laughrea, 1985; reviewed by Richardson, 1981; Richardson and Birchenall-Sparks, 1983; Richardson et al, 1983). A similar pattern was observed in the white leghorn chicken (Yang et al, 1977).…”

Section: Transcription and Translation In The Aging Brainmentioning

confidence: 99%

“…A similar pattern was observed in the white leghorn chicken (Yang et al, 1977). There is some disagreement pertaining to the exact time course of the decline, with some finding a greater rate of decline in translation during adulthood (Ekstrom et al, 1980; Fando et al, 1980; Ingvar et al, 1985; Smith et al, 1995), and others finding the greatest rate of decline during senescence (Dwyer et al, 1980). Similarly, although protein synthesis decline has been observed in many other types of tissues and cells (e.g., liver, kidney, muscle), the time courses and rates of decline vary (reviewed by Webster, 1985).…”

Section: Transcription and Translation In The Aging Brainmentioning

confidence: 99%

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Neural protein synthesis during aging: effects on plasticity and memory

Schimanski

Barnes

2010

Fronti.Ag.Neurosci.

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During aging, many experience a decline in cognitive function that includes memory loss. The encoding of long-term memories depends on new protein synthesis, and this is also reduced during aging. Thus, it is possible that changes in the regulation of protein synthesis contribute to the memory impairments observed in older animals. Several lines of evidence support this hypothesis. For instance, protein synthesis is required for a longer period following learning to establish long-term memory in aged rodents. Also, under some conditions, synaptic activity or pharmacological activation can induce de novo protein synthesis and lasting changes in synaptic transmission in aged, but not young, rodents; the opposite results can be observed in other conditions. These changes in plasticity likely play a role in manifesting the altered place field properties observed in awake and behaving aged rats. The collective evidence suggests a link between memory loss and the regulation of protein synthesis in senescence. In fact, pharmaceuticals that target the signaling pathways required for induction of protein synthesis have improved memory, synaptic plasticity, and place cell properties in aged animals. We suggest that a better understanding of the mechanisms that lead to different protein expression patterns in the neural circuits that change as a function of age will enable the development of more effective therapeutic treatments for memory loss.

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Section: Transcription and Translation In The Aging Brainmentioning

confidence: 99%

Section: Transcription and Translation In The Aging Brainmentioning

confidence: 99%

Neural protein synthesis during aging: effects on plasticity and memory

Schimanski

Barnes

2010

Fronti.Ag.Neurosci.

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“…A 20% decrease of mean CPSR was measured due to ageing in the brain of 11 to 26 month-old Wistar rats. This impairment (-18% to -37%) was conf i e d by measurements of the brain metabolism of L-leucine in rat (Ekstrom et al, 1980;Fando et al, 1980;Ingvar et al, 1985) based on different models. Our results, the absolute ROI CPSR values given in table I for the two control groups, were also confirmed by other similar studies with [35S]-L-methionine (Lestage et Williams et al, 1994).…”

Section: Effect Of Aging On Cpsrmentioning

confidence: 80%

Restoration of brain protein synthesis in mature and aged rats by a DA agonist, piribedil

Bustany

Trenque

Crambes

et al. 1995

Fundamemntal Clinical Pharma

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Summary— Brain ageing affects numerous cerebral metabolic pathways such as cerebral glucose consumption or protein synthesis rate. The pharmacological effect of a mixed D1‐D2 dopaminergic agonist, piribedil, on this last metabolism is reported. Cerebral Protein Synthesis Rate (CPSR) was measured by the [35S]L‐methionine autoradiographic procedure in 38 main brain regions of 11 and 26‐month‐old Wistar rats after a 2‐month treatment per os at 9 and 30 mg/kg/day with piribedil. Mean decrease of CPSR was −21% during the 15‐month ageing we followed, with important local variations. Mean CPSR increased with the two treatments, +25% in mature and +35% in aged rats. Treatments restored CPSR of aged rats to the exact mature subjects levels in quite all the brain regions. No dose‐effect or asymetrical modification was statistically revealed for the two treatments. Metabolic increases involved particularly central brain gray structures, especially some DA‐targeted brain nuclei concerned with behaviour and learning. This effect argued for a general metabotrophic effect of D1‐D2 dopamine stimulation of the brain. The original pattern of local ageing of brain protein synthesis in rat was also incidentally reported. This was the first direct report of a wide and effective metabolic activation of CPSR in the brain during ageing by a curative dopaminergic agonist treatment.

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“…In contrast, hepatic tissue basal levels of NAT-1 decreased with age. It is not known whether these changes would contribute to the age-related decrease in cerebral protein synthesis (28,29) or the age-related increase in hepatic protein synthesis (30,31).…”

Section: Resultsmentioning

confidence: 99%

Novel translational repressor (NAT-1) expression is modified by thyroid state and age in brain and liver

Shah

Mooradian

1998

European Journal of Endocrinology

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The technique of reverse transcriptase-polymerase chain reaction differential display was used to identify thyroid hormone (TH) responsive mRNAs in the adult rat cerebral tissue. A partial cDNA (0.76 kb) was cloned and sequenced. Comparison of the sequence to the GenBank data base showed almost 100% homology to mouse translational repressor (NAT-1) mRNA 3 0 -end. In a northern blot analysis this cDNA hybridized with a mRNA whose expression in hyperthyroid rat cerebral tissue was approximately 6-fold higher than in euthyroid rats. The time course studies showed a rapid induction of this mRNA within 3 h following thyroxine administration. This mRNA is widely expressed in various tissues, and in hepatic tissue it is also TH responsive.To determine if TH responsiveness of this mRNA persists during aging, 25-month-old aged rats were studied and the results were compared with those of 4-month-old rats. Unlike young mature rats, the TH responsiveness of NAT-1 mRNA in both the cerebral and hepatic tissue of aged rats was blunted. It is concluded that cerebral tissue in aging rats beyond the developmental stages, like the hepatic tissue, is associated with altered TH responsiveness.

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Age-dependent changes in brain protein synthesis in the rat

Cited by 54 publications

References 46 publications

Neural protein synthesis during aging: effects on plasticity and memory

Neural protein synthesis during aging: effects on plasticity and memory

Restoration of brain protein synthesis in mature and aged rats by a DA agonist, piribedil

Novel translational repressor (NAT-1) expression is modified by thyroid state and age in brain and liver

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