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Biomedical subjects

C G Wasterlain

Publications and source records attributed to C G Wasterlain.

At least 145 records · Page 8Linked to original sources
PubMed1976

Effects of neonatal status epilepticus on rat brain development.

A single, 2-hour episode of status epilepticus induced by flurothyl (1,500 mul) in 4-day-old rats irreversibly curtailed brain weight and brain DNA. Status epilepticus inhibited DNA synthesis but did not increase DNA breakdown and produced no histologic lesions. Rats with status epilepticus showed delayed behavioral milestones and reduced seizure thresholds several weeks after status. After milder convulsions (flurothyl 750 mul, bicuculline), brain DNA was curtailed at 7 days but returned to normal at 30 days. These results suggest that, in the immature brain, epileptic seizures too mild to cause cell necrosis can inhibit DNA synthesis and permanently curtail brain DNA content. This may account for the great vulnerability of the immature brain to epileptic seizures.

Animals↗
PubMed1976

Developmental effects of seizures: role of malnutrition.

Eighty-eight rats were paired at birth according to sex and weight. One member of each pair received two electroconvulsive seizures a day during the neonatal period (days 2 to 11). Access of its control littermate to the mother was restricted so that the body weights of any two paired rats never diverged by more than 2 gm on any day of life, and were usually within one half gram of each other. This guaranteed that the nutritional status of seizure-treated and control animals was similar throughout development. On day 30 of life, seizure-treated rats had smaller brains (-56 mg, P less than .05) and reduced numbers of brain cells (-13.10(6), P less than .05) compared to their control littermates. It was concluded that the reduction of brain DNA brought about by neonatal seizures was not simply caused by malnutrition of seizure-treated animals.

Animals↗
PubMed1975

Treatment of "on-off effect" with a dopa decarboxylase inhibitor.

Irregularities in motor response after continuing levodopa therapy of Parkinson disease (the "on-off effect") were assessed with the addition of L-alpha-methyldopa hydrazine (carbidopa) in a double-blind study. Thirteen of 20 patients improved while receiving carbidopa and levodopa while only four of 17 patients improved while receiving placebo and levodopa. Twenty-three of 37 patients improved in a subsequent non-blind trial of carbidopa plus levodopa. Improvement was not dependent on an increase in dose or frequency of levodopa administration. Adverse effects included dyskinesia, imbalance, and confusion; nausea was eliminated. On patient died of glomerulonephritis that predated the drug trial, but worsened progressively during and after it. Carbidopa's suppression of the "on-off effect" suggests that extracerbral factors may be important in this phenomenon.

Aged↗
PubMed1975

Developmental brain damage after chemically induced epileptic seizures.

25 Wistar rats were subjected twice daily to epileptic seizures induced by the convulsant gaz Flurothyl. Compared with littermates of the same sex and birth weight, the brain of seizure-treated rats showed a reduction of 6% (5.2 million cells) after 5 days and 17.6% (33.4 million cells) after 10 days of treatment.

Animals↗
PubMedDate not supplied

Regulation of type-II calmodulin kinase: functional implications.

Calmodulin-kinase II (CaM kinase) is a calcium/calmodulin-dependent protein kinase which is highly enriched in the nervous system and mediates many of calcium's actions. Regulation of CaM kinase activity plays an important role in modulating synaptic transmission, synaptic plasticity and in neuropathology. Primary regulation of CaM kinase occurs via changes in intracellular calcium concentrations. Increased calcium stimulates protein kinase activity and induces autophosphorylation. Autophosphorylation of CaM kinase at specific sites results in altered activity and responsiveness to subsequent changes in calcium concentrations. Intracellular translocation of CaM kinase also appears to result from autophosphorylation. These mechanisms of regulation play an important role in synaptic plasticity (e.g., Aplysia ganglia), status epilepticus and cerebral ischemia. Long-lasting alterations in the expression of CaM kinase have been demonstrated in the kindling model of epilepsy and in monocular deprivation and therefore modulation of gene expression, in addition to autophosphorylation and translocation, appears to be another important mechanism of regulating CaM kinase activity.

Animals↗