Daily Changes of Plasma Corticosterone by an 8-h Daytime Feeding Occur Without Body Weight Loss or Severe Food Restriction in the Rat

Different studies have reported that daytime feeding entrains the circadian rhythm of corticosterone secretion in rats. However, it remained unclear whether calorie restriction or daytime feeding access have an effect. The aim of our study is to evaluate the effect of an 8-h daytime feeding access on the circadian rhythm of plasma corticosterone. Eleven adult male Wistar rats were assigned to two different conditions of access to food: ad lib feeding for one week and daytime feeding for the following two weeks. On the 7th, 14th and 21st day, blood samples were collected every 4 h from 08:00 to 04:00. Food intake and body weight were recorded daily. During daytime feeding, rats ingested 88% of the amount of food ingested over 24 h in the ad lib feeding period. However, body weight increased significantly from the first day to the end of experiment. Peak plasma corticosterone was 12 h shifted during daytime feeding period compared to the ad lib condition. This study showed that an 8-h daytime feeding entrained the circadian rhythm of plasma corticosterone without body weight loss or severe food restriction.     

Daily Changes of Plasma Corticosterone by an 8-h Daytime Feeding Occur Without Body Weight Loss or Severe Food Restriction in the Rat

Different studies have reported that daytime feeding entrains the circadian rhythm of corticosterone secretion in rats. However, it remained unclear whether calorie restriction or daytime feeding access have an effect. The aim of our study is to evaluate the effect of an 8-h daytime feeding access on the circadian rhythm of plasma corticosterone. Eleven adult male Wistar rats were assigned to two different conditions of access to food: ad lib feeding for one week and daytime feeding for the following two weeks. On the 7th, 14th and 21st day, blood samples were collected every 4 h from 08:00 to 04:00. Food intake and body weight were recorded daily. During daytime feeding, rats ingested 88% of the amount of food ingested over 24 h in the ad lib feeding period. However, body weight increased significantly from the first day to the end of experiment. Peak plasma corticosterone was 12 h shifted during daytime feeding period compared to the ad lib condition. This study showed that an 8-h daytime feeding entrained the circadian rhythm of plasma corticosterone without body weight loss or severe food restriction.     

Synaptic Vesicle Ultrastructural Changes in the Rat Hippocampus Induced by a Combination of α-Linolenate Deficiency and a Learning Task

Abstract: Rats fed either a safflower oil (α-linolenate-deficient) or a perilla oil (α-linolenate-sufficient) diet through two generations (F1) showed significant differences in the brightness-discrimination learning task. In this task, correct responses were lever-pressing responses, which were reinforced with dietary pellets, and incorrect responses were those with no reinforcement. The inferior learning performance in the safflower oil group was caused mainly by the inferior ability to rectify the incorrect responses through the learning sessions. In the safflower oil group after the learning task, the average densities of synaptic vesicles in the terminals of the hippocampus CA1 region were decreased by nearly 30% as compared with those in the perilla oil group, and it is notable that this difference was not detected without the learning task. These results suggest that dietary oil-induced morphological changes in synapses in the hippocampus of rats are related to the differential learning performance and that the turnover rate of synaptic vesicles in the hippocampus may be an important factor affecting learning performance.     

In Vivo Changes in γ-Aminobutyric Acid Output from the Cerebral Cortex Induced by Inhibitors of γ-Aminobutyric Acid Uptake and Metabolism

Abstract: The effects of inhibitors of γ-aminobutyric acid (GABA) metabolism or uptake on GABA output from the cerebral cortex was studied by means of a collecting cup placed on the exposed cortex of rats anaesthetized with urethane. GABA was identified and quantified by a mass-fragmentographic method. Ethanolamine-O-sulphate (10⁻² M ) applied directly on the cerebral cortex caused a long-lasting twofold increase in GABA output, whereas dl -2, 4-diaminobutyric acid (5 × 10⁻³ M ) caused a sevenfold increase and β -alanine was inactive. The results indicate that glial uptake has little effect on GABA inactivation in the cerebral cortex. The inhibition of neuronal uptake seems a more effective tool to increase GABA concentration in the synaptic cleft, and consequently also in GABA output, than the inhibition of GABA metabolism.     

The Trp64Arg Polymorphism of the β3‐Adrenergic Receptor Gene Is Not Associated with Training‐Induced Changes in Body Composition: The HERITAGE Family Study

Objective: To investigate the association between the Trp64Arg polymorphism of the β3‐adrenergic receptor gene and changes in body composition in response to endurance training. Research Methods and Procedures: Adult sedentary white and black subjects participating in the HERITAGE Family Study were measured before and after 20 weeks on endurance training for the body mass index, fat mass, percentage of body fat, fat‐free mass, sum of eight skinfolds, and subcutaneous, visceral, and total abdominal fat areas. The association between the Trp64Arg polymorphism and the response phenotypes, computed as the difference between pre‐ and post‐training values, was tested by analysis of covariance separately in men and women. The gene by race interaction term was also tested. Results: No race differences were observed for allelic and genotype frequencies. Training resulted in significant reduction of body fat in both men and women. No association of the Trp64Arg polymorphism was observed with training‐induced changes for any of the body composition phenotypes in both men and women. Discussion: These results suggest that the Trp64Arg polymorphism of the β3‐adrenergic receptor gene is not related to changes in body composition in response to exercise training.     

Changes in the Amino Acid Content of Nerve Endings (Synaptosomes) Induced by Drugs that Alter the Metabolism of Glutamate and γ-Aminobutyric Acid

The study was centered on the changes in the amino acid content of nerve endings (synaptosomes) induced by drugs that alter the metabolism of glutamate or gamma-aminobutyric acid (GABA), and that possess convulsant or anticonvulsant properties. The onset of seizures induced by various convulsant agents was associated with a decreased content of GABA and an increased content of glutamate in synaptosomes. The concurrent administration of pyridoxine prevented both the biochemical changes and the convulsions. The administration of gabaculine to mice resulted in large increases in the GABA content of synaptosomes that were counteracted by decreases in glutamate, glutamine, and aspartate levels such that the total content of the four amino acids remained unchanged. The administration of aminooxyacetic acid (0.91 mmol/kg) resulted initially in seizure activity, but subsequently in an anticonvulsant action. No simple relationship existed between the excitable state of the brain induced by aminooxyacetic acid and the changes in the synaptosomal levels of any of the amino acid transmitters. A hypothesis was, however, formulated that explained the convulsant-cum-anticonvulsant action of aminooxyacetic acid on the basis of compartmentation of GABA within the nerve endings.     

Effects of Retigabine on the Neurodegeneration and Extracellular Glutamate Changes Induced by 4-Aminopyridine in Rat Hippocampus <Emphasis Type="Italic">In Vivo</Emphasis>

We have previously shown that microdialysis perfusion of the K⁺ channel blocker 4-aminopyridine (4-AP) in rat hippocampus induces convulsions and neurodegeneration, due to the stimulation of glutamate release from synaptic terminals. Retigabine is an opener of the KCNQ2/Q3-type K⁺ channel that possesses antiepileptic action and may be neuroprotective, and we have therefore studied its effect on the hyperexcitation, the neuronal damage and the changes in extracellular glutamate induced by 4-AP. Retigabine and 4-AP were co-administered by microdialysis in the hippocampus of anesthetized rats, with simultaneous recording of the EEG, and the extracellular concentration of glutamate was measured in the microdialysis fractions. In 70–80% of the rats tested retigabine reduced the 4-AP-induced stimulation of glutamate release and prevented the neuronal damage observed at 24 h in the CA1 hippocampal region. However, retigabine did not block the EEG epileptic discharges and their duration was reduced in only 20–25% of the tested animals. We conclude that the neuroprotective action of retigabine is probably due to the blockade of the 4-AP-induced stimulation of glutamate release. This inhibition, however, was not sufficient to block the epileptic activity. Special issue dedicated to Dr. Simo S. Oja