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Biomedical subjects

G Pepeu

Publications and source records attributed to G Pepeu.

At least 181 records · Page 10Linked to original sources
PubMed1978

Effect of bromocriptine on acetylcholine output from the cerebral cortex.

The effect of bromocriptine on acetylcholine (ACh) output from the cerebral cortex was investigated in anaesthetized rats. Bromocriptine caused a brief decrease in ACh output at the dose of 0.1 mg/kg i.p. and a dose-related long-lasting increase at doses from 1.25 to 10 mg/kg i.p. Apomorphine elicited an increase in ACh output when injected intraperitoneally at doses from 0.1 to 10 mg/kg. When bromocriptine was administered to rats in which a septal lesion had been made 12 days prior to the test, no increase in ACh output was observed. Bromocriptine seems therefore to stimulate a cortical cholinergic pathway originating from or passing through the septum.

Acetylcholine↗
PubMed1978

Drug effect on cholinergic mechanisms in the cerebral cortex.

Investigations aimed to define the components of the cholinergic network in the cerebral cortex and their functional modifications under the effect of a number of psychotropic drugs are described. By measuring acetylcholine levels and acetylcholine output from the cerebral cortex in cats and rats with various subcortical lesions, at least two systems of cholinergic neurons ascending to the cortex were demonstrated. One of the systems originates from the septum and its activity is affected by drugs acting on dopaminergic receptors.

Acetylcholine↗
PubMed1976

Investigations into the relationship between phospholipids and brain acetylcholine.

The effect of a phospholipid mixture extracted from the bovine cerebral cortex and of pure phosphatidylserine (PS), phosphatidylethanolamine (PE) and phosphatidylcholine (PC) on ACh output from the cerebral cortex was investigated in rats anaesthetized with urethane. All the phospholipids were administered after sonication. ACh was determined by bioassay. The following results were obtained: after i.p. administration of 100 mg/kg of the phospholipid mixture a marked increase in ACh output I asting approximately 30 min was observed. The i.v. administration of PS caused a dose-dependent increase in ACh. At the dose of 150 mg/kg a 3-fold increase over the spontaneous ACh output was found. PE was less active than PS and PC showed no effect on ACh output. The possibility that PS and PE might increase ACh output through a mechanism facilitating Ca penetration is discussed.

Acetylcholine↗
PubMed1976

Changes in regional brain acetylcholine levels during drug-induced convulsions.

Acetylcholine (ACh) levels were determined in the brain of rats killed by decapitation or focussed microwave radiation during drug-induced convulsions. During metrazol or strychnine-induced convulsions a diffuse decrease in ACh levels was found in rats killed by decapitation. When the rats were killed by radiation and the brain was only divided into three large regions, strychnine caused no changes in ACh levels; metrazol caused a decrease in the cerebral cortex and lower brainstem. When discrete brain regions were investigated in rats killed by radiation, metrazol-induced convulsions were associated with a decrease in ACh level in all regions dissected and strychnine-induced convulsions with a decrease in the hippocampus and caudate nucleus only. Picrotoxin-induced convulsions were associated with a decrease in ACh level in the cerebral cortex, hippocampus, midbrain and medulla-pons, those induced by bicuculline with an increase in ACh level in the frontal cortex, hippocampus, midbrain and medulla-pons, by dimefline with an increase in the frontal cortex, midbrain and medulla-pons and a decrease in the caudate nucleus. The experiments show that each type of convulsant affects ACh levels in discrete brain regions in a different way.

Acetylcholine↗