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Biomedical subjects

N Bertrand

Publications and source records attributed to N Bertrand.

At least 55 records · Page 3Linked to original sources
PubMed1994

Interaction between histamine and adenosine in human cerebromicrovascular endothelial cells: modulation of second messengers.

This study demonstrates the presence of histamine H1 and H2 receptors and purinoreceptors A1 and A2 on endothelial cells derived from human brain microvessels (HBEC). Histamine induced formation of both inositol triphosphate (IP3) (EC50 = 10.2 +/- 0.9 microM) and cyclic adenosine monophosphate (cAMP) (EC50 = 5.2 +/- 0.9 microM) in HBEC in a concentration-dependent fashion. IP3 formation was inhibited by H1 receptor antagonists mepyramine maleate and chlorphenyramine, but not by H2 receptor antagonist cimetidine. Production of cAMP was efficiently inhibited by cimetidine. Selective A1 receptor agonists decreased, whereas A2 receptor agonists increased cAMP production in HBEC. When added together with histamine to HBEC cultures, both A1 and A2 receptor agonists diminished histamine-induced IP3 stimulation. This effect was reversed in the presence of specific A1 and A2 receptor antagonists, respectively. Marked augmentation of histamine-induced cAMP production by HBEC was observed in the presence of A2 agonist. This response was dependent on H1 receptors, since it was reduced in the presence of H1-receptor antagonist. It is suggested that interaction between histamine and adenosine modulating induction of second messengers in HBEC may influence endothelium-dependent responses of brain microvascular compartments.

Adenosine↗
PubMed1994

Brain fixation for acetylcholine measurements.

Brain fixation using a commercially available microwave oven (power output: 750 W) has been investigated as a means for enzyme inactivation preventing post-mortem changes in brain acetylcholine (ACh) and choline (Ch) levels. Rats and mice were decapitated, and the severed heads immediately irradiated for 5.5 and 3 s, respectively, resulting in a complete inactivation of brain acetylcholine esterase (AChE) and choline acetyltransferase (ChAT). The ACh and Ch contents measured in various brain regions of rat and mouse were: (in rat) striatum 60.5 and 32.4 nmol/g, hippocampus 20.4 and 30.9 nmol/g, cortex 24.2 and 19.6 nmol/g; (in mouse) striatum 70 and 47.2 nmol/g, hippocampus 22. 1 and 30.2 nmol/g, cortex 22.9 and 27.9 nmol/g. These values were found in accordance with those reported in the literature by irradiating whole animals in instruments of higher power capabilities. Thus, the procedure described in the present work may be a simple and valuable means of brain fixation for neurochemical studies of brain ACh in small animal species.

Acetylcholine↗
PubMed1993

Endothelins release 51Cr from cultured human cerebromicrovascular endothelium.

The effects of vasoactive peptides endothelins (ET-1, ET-2, ET-3, S6b, S6c) on release of 51Cr, production of inositol triphosphate (IP3), and release of arachidonic acid (AA) were examined in cultured microvascular endothelium derived from human brain (HBEC). ET-1 induced dose-dependent release of 51CR (EC50 = 7 +/- 2 nM), transient increase of IP3 (EC50 = 0.67 +/- 0.09 nM), and sustained release of AA (EC50= 59 +/- 7 nM) from HBEC. Under the same experimental conditions, viability of the cells was preserved (> 97%) as assessed by exclusion of vital dye trypan blue and release of lactate dehydrogenase (LDH). Dexamethasone (1 microM) inhibited ET-1-induced AA release, whereas it was ineffective on 51Cr release. Protein kinase C (PKC) inhibitor H7 (200 nM), calcium channel blocker verapamil (10 microM), or IP3 receptor antagonist ryonidine (5 microM) reduced ET-1 (100 nM)-induced release of 51Cr. These findings indicate that endothelins can induce an increase of HBEC permeability by a receptor-specific activation of PKC and intracellular calcium mobilization.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Biphasic striatal acetylcholine release during and after transient cerebral ischemia in gerbils.

Acetylcholine (ACh) release into the extracellular space was measured by HPLC with electrochemical detection after in vivo intracerebral microdialysis in the striatum of gerbils subjected to 15 min of bilateral carotid artery occlusion followed by 5 h of recirculation. Tissue ACh and choline (Ch) contents were also determined during ischemia and after 5, 30, 60, and 120 min of reflow. Fifteen minutes of ischemia led to a significant transient increase in extracellular ACh concentration (threefold after 7.5 min of ischemia) concomitant with a reduced endogenous ACh level (-62%) and increased tissue Ch content (ninefold). Recirculation significantly reduced the ACh release during the early period of reflow (-50% vs. basal level), followed by a significant increase in ACh release between 1 and 3 h of reflow (45-55% vs. basal level) and subsequent normalization. Simultaneously, a "rebound" of tissue ACh level occurred in the early period of reflow (fourfold vs. ischemic value), followed by gradual normalization after 2 h of reperfusion, whereas a rapid decrease in tissue Ch levels was found after 30 min of reflow. These findings represent the first demonstration of a biphasic release of ACh during ischemia and reperfusion, as assessed by intracerebral microdialysis in gerbils.

Acetylcholine↗
PubMed1992

Regional and temporal glycerol changes induced by forebrain ischemia in gerbils.

Temporal ischemic changes in glycerol and energy metabolites were studied in the striatum, hippocampus and cortex of gerbils subjected to 15 min of bilateral carotid artery occlusion alone or with various periods of recirculation. The same tissue sample served for the determination of glycerol and energy reserve by a simple enzymatic fluoro- and spectrometric assay after perchloric acid extraction. Cerebral ischemia increased the levels of glycerol (8- to 10-fold) and depleted the energy stores. During the first hour of recirculation, the glycerol content decreased and thereafter (at 2 h), normalized in all structures. However, the glycerol content was still twice as high in the striatum and hippocampus as compared to their respective controls. At the same time, an incomplete restoration of energy reserves was observed in these structures. The findings indicate that glycerol is not a stable postischemic indicator of the ischemia-induced membrane damage.

Adenosine Triphosphate↗
PubMed1992

Post-ischemic regional changes in acetylcholine synthesis following transient forebrain ischemia in gerbils.

The synthesis rate of brain acetylcholine (ACh) was estimated 30 min and 5 days following transient forebrain ischemia performed by 10 min bilateral carotid occlusion in gerbils. ACh synthesis was evaluated from the conversion of radiolabeled choline (Ch) into ACh after an i.v. administration of [methyl-3H]Ch. Endogenous and labeled Ch and ACh were quantified by HPLC. The synthesis rate of Ach was significantly decreased following 30 min of recirculation. The reductions reached 55.4% in the hippocampus, 51.2% in the cerebral cortex and 44.4% in the striatum. Five days after ischemia, the values returned to normal in the cerebral cortex and in the striatum, while ACh synthesis remained selectively lowered (-30.4%, p less than 0.01) in the hippocampus. These cholinergic alterations may account for both early and delayed post-ischemic behavioral and mnesic deficits.

Acetylcholine↗
PubMed1991

Cerebral ischemia: changes in brain choline, acetylcholine, and other monoamines as related to energy metabolism.

The relationship of cerebral neurotransmitters acetylcholine (ACh), noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5HT) to the energy state of the brain was examined in mice at various times following complete ischemia produced by decapitation, in gerbils submitted to transient global ischemia (10 min bilateral carotid artery occlusion, 5 or 30 min recirculation), and in rats 24 hr after irreversible microembolism. Ischemia caused significant reductions in brain monoamine concentrations. The alterations in NA, DA, and 5HT levels persisted during recirculation and were unrelated to energy restoration. They were accompanied by an increase in the concentrations of related metabolites, suggesting that synthesis was unable to compensate for the release of the transmitters at early post-ischemic time periods. As described for the catecholamines and 5HT, ischemia resulted in a significant decrease in ACh level, but recirculation was associated with a rapid increase in ACh concentration. Impaired synthesis and/or increased release of ACh can be responsible for the decrease in ACh concentration during ischemia. Early post-ischemic elevation of ACh may be related to the large increase in brain choline brought about by ischemia.

Acetylcholine↗
PubMed1990

Effect of oxotremorine, physostigmine, and scopolamine on brain acetylcholine synthesis: a study using HPLC.

The synthesis rate of brain acetylcholine (ACh) was estimated in mice following i.v. administration of [3H]choline (Ch). The measurements were performed 1 min after the tracer injection, using the [3H]ACh/[3H]Ch specific radioactivity ratio as an index of ACh synthesis rate. Endogenous and labeled Ch and ACh were quantified using HPLC methodology. Oxotremorine and physostigmine (0.5 mg/kg, i.p.) increased the steady state concentration of brain ACh by + 130% and 84%, respectively and of Ch by + 60% (oxotremorine); they decreased ACh synthesis by 62 and 55%, respectively. By contrast, scopolamine (0.7 mg/kg, i.p.) decreased the cerebral content of Ch by - 26% and of ACh by - 23% without enhancing the synthesis of ACh. The results show the utility of HPLC methodology in the investigation of ACh turnover.

Acetylcholine↗
PubMed1990

Turnover rate of brain acetylcholine using HPLC separation of the transmitter.

A simple, reliable method was developed for measuring brain acetylcholine (ACh) turnover using HPLC methodology. Mice were injected intravenously with [3H]choline ([3H]Ch), and the turnover rate of ACh was calculated from the formation of [3H]ACh. Ch and ACh were separated from phosphorylcholine and from other radioactive compounds using tetraphenylboron extraction and counterion/reverse-phase chromatography. Endogenous Ch and ACh were quantified electrochemically through hydrogen peroxide production in a postcolumn reactor containing covalently bonded ACh esterase and Ch oxidase. Labeled Ch and ACh were quantified in the same sample by collecting the chromatographic fractions for radioactive content determinations. The method is rapid, well adapted to large series, and highly reproducible, with recoveries of 72.1% for Ch and 79.3% for ACh. The turnover value in mouse cerebral hemispheres was 16.02 nmol g-1 min-1 and decreased to 9.94 nmol g-1 min-1 in mice treated with oxotremorine.

Acetylcholine↗
PubMed1977

[Blood xylose as a screening test for malabsorption in jejunal mucosa abnormalities; importance of diet in interpretation].

Blood xylose level 60 min. after an oral dose of 10 g/m2 xylose was compared with the histology of the jejunal mucosa in 56 children. Ninety-two percent of children with blood xylose below 20 mg/100 ml had an abnormal jejunal mucosa; 98% of children with a normal mucosa had a blood xylose above 20 mg/100 ml. In children with coeliac disease the following observations were made: 1) blood xylose was above 20 mg/100 ml in 50% of children with flat mucosa; all were given a diet excluding gluten; 2) blood xylose levels which were initially below 20 mg/100 ml were found above this level 3 to 12 days after the onset of the diet; 3) all the histological relapses following re-introduction of gluten in the diet were not associated with a decrease of blood xylose level below 20 mg/100 ml.

Adolescent↗
PubMedDate not supplied

DHA-enriched phospholipid diets modulate age-related alterations in rat hippocampus.

Our previous work on rat hippocampus showed that a loss of docosahexaenoic acid (DHA) occurs in the fatty acid composition of phosphatidylethanolamine (PE), plasmenylethanolamine (PmE) and phosphatidylserine (PS) with increasing age. The present study investigated whether a DHA-enriched phospholipid dietary supplement could restore DHA levels and cholinergic activity. Male rats were fed a balanced diet containing both linoleic and alpha-linolenic acids until the age of 2, 18 and 21 months. From 18 to 21 months, one subgroup received a diet supplemented with DHA-enriched phospholipids from egg yolk (E-PL), and another a diet with DHA-enriched phospholipids from pig brain (B-PL). Compared to the control diet, the E-PL diet restored the proportion of polyunsaturated fatty acids (PUFAs: 22:6n-3 and 20:4n-6) in PE and PmE, while enhancing spontaneous and evoked-acetylcholine (Ach) release. The B-PL diet had no effect on PUFAs, but increased basal extracellular levels of Ach in 21-month-old rats as compared to the age-matched control. Our results show that supplementation with DHA-enriched egg PL can enhance Ach release and correct PUFA composition.

Acetylcholine↗