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C G Wasterlain

Publications and source records attributed to C G Wasterlain.

At least 127 records · Page 7Linked to original sources
PubMed1980

Age-dependent changes in brain protein synthesis in the rat.

Brain protein synthesis was studied in vivo, in brain slices, and in cell-free systems in rats aged 1, 16, and 24 months. We observed a highly significant reduction in amino acid incorporation with advancing age. This reduction was observed in vivo, in slices, in postmitochondrial supernatant, microsomes, and membrane-bound polysomes. Free heavy polysomes showed no age-dependent decline but formed a smaller proportion of total ribosomes in older animals. These studies suggest that in the rat brain protein synthesis declines before senescence, possibly due to an impairment in the initiation process.

Age Factors↗
PubMed1980

A simple reproducible cell-free system for measuring brain protein synthesis.

A simple, rapid, sensitive, and reproducible cell-free assay system for studying brain protein synthesis is described. This system uses small amounts of brain postmitochondrial supernatant, making it a convenient screening test when only small amounts of tissue are available. It showed over 95% dependence on Mg2+ and on an energy source. Optimal incorporation occurred under the following conditions: Mg2+ 3 mM; ATP, 0.6 mM; GTP, 0.6 mM; high K+, greater than or equal to 25 mM; Low Na+, less than or equal to 15 mM; pH 7.1-7.5. The rate of amino acid incorporation did not vary with leucine concentrations in vitro up to 1 mM, which obviated the need to measure endogenous leucine concentrations.

Adenosine Triphosphate↗
PubMed1980

Aging and rat brain muscarinic receptors as measured by quinuclidinyl benzilate binding.

Measurement of cholinergic muscarinic receptor binding in various rat brain areas using the ligand [3H]quinuclidinyl benzilate indicates that receptor binding is decreased in striatum and cerebellum of aged female rats (22 months old) as compared to younger rats (4 months old). Decreases were not observed in cortex, hippocampus, hypothalamus, or amygdala areas. Further examination o [3H]quinuclidinyl benzilate binding in subcellular fractions of aged and young rat cerebellum and striatum indicated a decrease in binding in the crude nuclear and crude synaptosomal fractions. Binding data indicate the observed decrease in specific ligand binding is due to a decrease in number of binding sites while receptor affinity does not appear to change.

Acetylcholinesterase↗
PubMed1980

Rat brain protein synthesis declines during postdevelopmental aging.

Using improved methods to measure brain protein synthesis in vivo (Dunlop et al., 1975) we have established that brain protein synthesis significantly declines in forebrain, cerebellum and brain stem when mature rats (3 months old) are compared to old rats (22.5 months old). The incorporation of (3H) L-lysine into forebrain protein is reduced 11% in 10.5 month old rats compared to 3 month old rats. A further reduction of 9% occurred between 16.5 months and 22.5 months. Our data suggest that reduced levels of protein synthesis initiation may be responsible, at least in part, for this age-related decline.

Aging↗
PubMed1980

Synaptic proteins after electroconvulsive seizures in immature rats.

The forebrain content of several rat brain synaptic proteins (synaptin, D1, D2, and D3) was reduced in rats receiving electroconvulsive seizures on days 2-11, 9-18, or 19-28 and sacrificed at the age of 30 days. Forebrain weight, total protein, and the glial enzyme glutamine synthetase were also decreased, whereas the neuronal enolase 14-3-2 was unchanged. The findings suggest that seizures in the immature rat brain resulted in a parallel reduction of synaptic material and of the amount of glial cells. The increased concentration of the enolase 14-3-2 found in rats seizured on days 19-28 may reflect the high demands on the glycolytic system during the seizures.

Animals↗
PubMed1979

Does anoxemia play a role in the effects of neonatal seizures on brain growth? An experimental study in the rat.

Groups of 4 Wistar rat littermates of matched sex and weight received the following daily treatment between the ages of 2 and 11 days: handling (untreated controls, UC), succinylcholine paralysis and ventilation with 100% O2 (respirator control, RC), electroconvulsive seizures (ECS) and ECS while paralyzed and ventilated with O2 (respirator seizures, RS). Analysis of heart blood O2 content showed that mechanical ventilation with 100% O2 effectively prevented the anoxemia observed during convulsive seizures. In the ECS and RS groups, several behavioral milestones (e.g. swimming) matured later than they did in either control group (UC, RC). No difference was observed between the two groups of seizure-treated rats. At the age of 30 days, both ECS and RS groups had smaller brains with a reduced DNA, RNA, protein and cholesterol content in both forebrain and hindbrain, suggesting that seizures curtailed the number of brain cells. The lack of any difference between the two seizure groups suggests that at least part of the adverse effects of experimental neonatal seizures on brain and behaviour are independent of anoxemia.

Animals↗
PubMed1978

Chronic inhibition of brain protein synthesis after portacaval shunting. A possible pathogenic mechanism in chronic hepatic encephalopathy in the rat.

We investigated the effects of chronic portacaval shunting, with or without additional ammonia loading, on brain protein synthesis in unanesthetized rats by continuous intravenous infusion of 3H-lysine (10 mumoles per gram, 0.2 muCi/mumole). Lysine was incorporated into forebrain proteins at a rate of 1.6 nanomoles/mg protein per hour in sham-operated controls, but at a rate of only 0.83 nanomoles/mg protein per hour (p less than 0.001) in paired rats 6 to 8 weeks after construction of a portacaval shunt. An acute load of ammonium acetate in portacaval-shunted animals further decreased the rate of lysine incorporation into forebrain proteins. Chronic inhibition of protein synthesis may play a role in the pathogenesis of chronic portacaval encephalopathy.

Ammonia↗
PubMed1977

Effects of neonatal seizures on ontogeny of reflexes and behavior. An experimental study in the rat.

18 newborn rats received two electroshock seizures daily for 10 days. Their neurochemical and behavioral development was compared to that of littermates fo the same sex and similar weight, which were either untreated or treated with the same total amount of electrical current at subconvulsive intensities. While the two control groups were behaviorially or neurochemically indistinguishable, experimental rats reached several behavioral milestones (swimming, free-fall righting, auditory startle, visual placing) significantly later than controls and had smaller brains, containing significantly less DNA, protein or cholesterol than either control group. This study demonstrates that in the rat neonatal seizures are followed not only by impaired neurochemical development of the brain but also by delays in the animal's behavioral development.

Animals↗
PubMed1976

Status epilepticus in immature rats. Protective effects of glucose on survival and brain development.

The role of glucose metabolism in alleviating the complications of status epilepticus (SE) was investigated in developing rats. Pretreatment with glucose reduced mortality from SE by 90% in rats under 1 week of age, 80% in 10-day-old rats, 50% in 15- to 20-day-olds, and not at all in adults. In 4-day-old animals, brain DNA synthesis during seizures, and in survivors, brain weight, DNA, RNA, protein, and cholesterol contents at 7 days of age were reduced less in glucose-treated than in saline-treated littermates. In the saline group, seizures caused a progressive fall in brain glucose level but no fall in blood glucose level, suggesting that glucose transport from blood to brain could not keep pace with glycolytic demands. In glucose-treated rats, blood and brain glucose concentrations remained elevated throughout the convulsive period. There was no reduction of brain adenosine triphosphate levels in either group. Thus, the protection by glucose appears to be related to its roles as a carbon source rather than an energy source. It is concluded that in immature animals, depletion of brain glucose can occur in the absence of hypoglycemia, and may be an important and potentially treatable complication of status epilepticus.

Adenosine Triphosphate↗