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S Nicolaidis

Publications and source records attributed to S Nicolaidis.

90 records · Page 5Linked to original sources
PubMed1976

The asymmetric distribution of enzymic activity between the six subunits of bovine liver glutamate dehydrogenase. Use of D- and L-glutamyl alpha-chloromethyl ketones (4-amino-6-chloro-5-oxohexanoic acid.

A method for the preparation of D- and L-glutamyl alpha-chloromethyl ketones (4-amino-6-chloro-5-oxohexanoic acid) is described. These chloromethyl ketones irreversibly inactivated bovine glutamate dehydrogenase, whereas several other related compounds had no adverse effect on the activity of the enzyme. The inactivation process was shown to be due to the modification of lysine-126. The time-courses for the inactivation and the incorporation of radioactivity from tritiated L-glutamyl alpha-chloromethyl ketone into the glutamate dehydrogenase were biphasic. The results were interpreted to suggest the involvement of 'negative co-operative' interactions in the reactivity of lysine-126. From the cumulative evidence it is argued that the first subunit of the enzyme, which takes part in catalysis, makes the largest, and the last the smallest, contribution to the overall catalysis. It is emphasized that three of the six subunits of the enzyme may possess as much as 80% of the total activity of bovine glutamate dehydrogenase.

Amino Acid Chloromethyl Ketones↗
PubMed1976

Effects of lithium chloride on sleep patterns in the rat.

Continuous EEG recordings were performed in rats both after saline injections (control days) and after LiCl treatments. LiCl administration was always followed by an initial period of general distress and sleep inhibition during 2 to 3 hr after low toxic doses (1.5 mEq/kg) and a much more longer period (10 hr) after high toxic doses (3 mEq/kg). Once this state was overcome, the pharmacological effect of lithimia seems to potentiate sleep and particularly paradoxical sleep (PS). It appears that this potentiation of PS occurs once lithimia reaches levels used in human therapeutics.

Animals↗
PubMed1975

Regulatory drinking in rats with permanent access to a bitter fluid source.

Male rats were given a quinine adulterated fluid as their sole source of liquid for over 60 days. After a latency of a few days, fluid intake stabilised at about 20 ml/day, with the water to food ratio close to 1.0 ml/g. Bodyweights fell to 90 percent of control levels (rats drinking unadulterated water). A battery of dipsogenic challenges was administered. Compared to controls, the ingestive responses during elevated ambient temperature, hyperosmotic salty food, after fluid deprivation, and to extracellular fluid depletion, were all attentuated. Drinking to acute NaCl injections was totally abolished. The intake of the adulterated fluid was near zero during food deprivation, and when a vegetable and fruit diet was available. Body fluid changes were suggestive of a net dehydration in the quinine drinking rats. Parallels with self intravenous drinking rats and rats recovered from lateral hypothalamic lesions were considered, and possible fundamental differences between natural and nonatural thirst stimuli.

Animals↗
PubMed1975

Metering of intravenously infused nutrients in VMH lesioned rats.

Rats were chronically implanted with lesioning electrodes in the ventromedial hypothalamus and with intracardiac catheters. The effects on ad lib oral food intake of a continuous intravenous infusion of glucose were studied both before and after lesioning. Before the lesion oral food intake was reduced by an average of 0.59 kcal per kcal infused. Postlesion the reduction of oral intake was correlated with the caloric value of the infusion, with a mean of 0.92 kcal per kcal. Rats with ventromedial hypothalamic lesions thus adjust their oral intakes in accordance with a systemically infused supplement. Further, the metering of systemically infused substrates actually appears to be more adequate after the lesion. This may be due to an exaggerated insulin release to systemic inputs which have bypassed the orogastric route and are thus unable to elicit preabsorptive endocrine reflexes.

Animals↗
PubMedDate not supplied

Parabrachial lesions disrupt responses of rats to amino acid devoid diets, to protein-free diets, but not to high-protein diets.

Normal rats "reduce" intake of diets that lack an essential amino acid (THR-DEV), are protein free (PO%), or contain a high proportion of protein (P75%). We tested the importance of the parabrachial nuclei (PBN) in signaling such adjustments of food intake by placing electrophysiologically guided lesions in these nuclei at points that responded to gustatory stimuli. When fed the THR-DEV diet, rats with PBN lesions (PBNx) decreased their food intake significantly less than the controls (78.5 vs. 44.4%). When put on a P0% diet, PBNx animals decreased their intake only 8% compared with 23% for our CONT group. When put on a P75% diet, however, both groups decreased their intake in an equivalent amount. These experiments show that the PBN is involved in the learned aversion to an amino acid devoid diet.

Amino Acids↗
PubMedDate not supplied

Determination, using microdialysis, of hypothalamic serotonin variations in response to different macronutrients.

In response to a chow meal in rats, we observed previously in PVN-VMH dialysates, an increase in serotonin (5-HT) that could be related to satiety or to metabolic consequences of the composition of the meal. Indeed, carbohydrates are admitted to increase 5-HT synthesis while proteins decrease it, but the time course and mechanisms of these effects were not known. For that purpose, pure carbohydrates, proteins, or fats were offered for 30 min and the changes in 5-HT from PVN-VMH dialysates were followed. Carbohydrates (85% starch + 15% sucrose) enhanced 5-HT levels as soon as the first 15 min of feeding, with a maximum 60 min later. Conversely, protein ingestion induced in the second 15 min of the meal, a decrease in 5-HT that lasted 2 h. During a fat meal (lard), 5-HT levels also decreased at the beginning of the meal and remained low during 45 min. The present data reassess the previous theories on the serotonergic effects of specific macronutrient ingestion. The effect of a fat meal on 5-HT levels had never been described so far. The increase in 5-HT in response to a carbohydrate meal is further specified. The 5-HT decrease induced by proteins, in agreement with the previous theories, is better explained now by using pure protein diets and extracellular 5-HT assay. However, all the changes observed start too early to be only metabolic in origin. Other mechanisms may occur, including the release of 5-HT in response to a meal to induce satiety.

Animals↗