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Biomedical subjects

C R Lee

Publications and source records attributed to C R Lee.

At least 73 records · Page 4Linked to original sources
PubMed1985

5-methoxytryptoline and close analogs as candidates for the endogenous ligand of the 3H-imipramine recognition site.

3H-Imipramine labels with high affinity a site associated with the macromolecular complex of the serotonin transporter in brain and platelets. There is a good correlation between the potencies of drugs at inhibiting 3H-5HT uptake and at inhibiting 3H-imipramine binding. Dissociation experiments indicate that the site labelled by 3H-imipramine is not identical with the substrate recognition site of the serotonin transporter and thus, it appears that 3H-imipramine labels a modulatory site for the 5HT transport system. On this basis, the existence of an endacoid acting on the 3H-imipramine recognition site to modulate 5HT uptake is discussed. The possibility that 5-methoxytryptoline or a closely related analog may be the endogenous ligand for the 3H-imipramine recognition site is analysed on the basis of the fact that 5-methoxytryptoline is a potent inhibitor of 3H-imipramine binding that also inhibits 3H-5HT uptake.

Binding, Competitive↗
PubMed1983

Dopamine receptors modulating [3H]acetylcholine release in slices of the cat caudate: effects of (-)-N-(2-chloroethyl)-norapomorphine.

(-)-N-(2-Chloroethyl)-norapomorphine [-)-NCA) inhibited in a concentration-dependent manner the electrically evoked [3H]acetylcholine release in slices of cat caudate. The inhibition by (-)-NCA was reversible and antagonized by the benzamide neuroleptic S-sulpiride. Although (-)-NCA is an irreversible antagonist at some behaviorally relevant postsynaptic dopamine receptors, its effect as an agonist on dopamine receptors modulating [3H]acetylcholine release strongly resembles its action on presynaptic dopamine autoreceptors modulating [3H]dopamine release. Our results suggest that the dopamine receptor modulating [3H]acetylcholine release may not be an appropriate in vitro model for those behaviorally relevant postsynaptic dopamine receptors which are antagonized by (-)-NCA. It is more likely that it conforms to the characteristics of presynaptic release-modulating dopamine autoreceptors. The agonistic action of (-)-NCA at presynaptic dopamine receptors, in contrast to the irreversible antagonism of some postsynaptic dopamine receptors by (-)-NCA, should be interpreted with caution. Evidence is presented which suggests that (-)-NCA breaks down in solution into (-)-N-(2-hydroxylethyl)-norapomorphine [-)-NHA). Since (-)-NHA is an agonist at presynaptic dopamine receptors, this physicochemical breakdown product may be partly responsible for the apparent agonistic properties of (-)-NCA under our in vitro conditions.

Acetylcholine↗
PubMed1983

Electrolyte metabolism in patients with periodic affective disorders during treatment with rubidium.

Five patients suffering from periodic affective disorders with short mood-cycles were treated with rubidium chloride, producing peak erythrocyte concentrations between 9 and 13 mmol/l. Loading with rubidium was associated with decreased total body potassium, but red-cell potassium was unchanged. Regular mood-cycling was disturbed, together with the associated body-weight changes. There was a slight extracellular "metabolic" acidosis. Electrolyte concentrations fluctuate abnormally in these patients, and two muscle biopsy specimens had very low potassium contents.

Affective Disorders, Psychotic↗
PubMed1982

Gas chromatographic mass spectrometric identification of O-demethylated and mono-hydroxylated metabolites of levomepromazine in blood from psychiatric patients by selected ion recording with high resolution.

An O-demethylated and two mono-hydroxylated metabolites of levomepromazine have previously been identified as conjugates in the urine from psychiatric patients. The three metabolites were identified in hydrolysed and nonhydrolysed plasma and erythrocytes from three patients by selected ion monitoring of the trimethylsilyl derivatives, with a mass spectrometric resolution of 5000. The three metabolites were mainly found as conjugates in the plasma, and smaller amounts were found unconjugated in the plasma and the erythrocytes.

Adult↗
PubMed1982

Noradrenergic neurotransmission in the brain of a convulsive mutant mouse, differences between the cerebral cortex and the brain stem.

The Quaking mouse is a genetically determined model of convulsive disorders. We investigated the modulation of noradrenergic neurotransmission through alpha 2-adrenoceptors in the occipital cortex and the brain stem of this mutant. The endogenous levels of noradrenaline were similar in the cerebral cortex of the Quaking mice and their corresponding controls, while a significant increase of endogenous noradrenaline was found in the brain stem of the mutants. The rate of disappearance of noradrenaline in the cerebral cortex and the brain stem after injection of FLA 63 was identical in control and Quaking mice. The calcium-dependent electrically evoked overflow of 3H-noradrenaline from slices of occipital cortex was inhibited by clonidine and enhanced by yohimbine in Quaking as well as in normal mice. The negative feed-back mechanism mediated by presynaptic alpha 2-adrenoceptors operates to a similar extent in both strains of mice. In contrast to the occipital cortex, in the brain stem, the amount of neurotransmitter released by electrical stimulation was significantly increased in Quaking mice when compared with controls. However, in the brain stem, the negative feed-back regulation of noradrenaline release operates to a similar extent in both strains of mice. When the endogenous levels of MOPEG were determined in the brain stem, they were found to be significantly higher in the Quaking mice when compared to the controls. The results suggest that an increase in noradrenergic neurotransmission in the brain stem, rather than in the cerebral cortex, could contribute to the behavioural abnormalities exhibited by the Quaking mice.

Animals↗
PubMed1980

The use of arginine analogues for investigating the functional organization of the arginine-binding site in lobster muscle arginine kinase. Role of the 'essential' thiol group.

1. The nature of arginine binding to lobster arginine kinase and the extent of its possible involvement with the ;essential' thiol group of the enzyme has been investigated with some inhibitory analogues of arginine. 2. Most of the analogues inhibit competitively, although mixed inhibition may occur if the alpha-carboxy group or alpha-amino group is absent. 3. The K(i) values indicate that strength of binding depends on the length of the carbon chain (l-isoleucine>l-valine>l- alpha-aminobutyrate>l-alanine) and the integrity of the substituents on the alpha-carbon atom (l-arginine>agmatine and l-ornithine>putrescine). The guanidino group probably contributes little to substrate binding, but a positive charge near the delta-nitrogen atom appears to be important (l-ornithine>l -citrulline>l-alpha-aminobutyrate). A cyclic analogue, 2-carboxymethyl-3-oxo-2,3,5,6,7,8-hexahydro-1H-imidazo [1,2-a][1,3]diazepine-8-carboxylic acid, has a low K(i) value similar to that of an equivalent straight-chain form, suggesting that arginine probably binds in a folded configuration. 4. The aliphatic l-amino acids give enzyme difference spectra similar to that with l-arginine and the integrity of the alpha-carboxy and alpha-amino groups appears to be a minimal but not sufficient requirement for this, as l-ornithine gives an atypical difference spectrum. A difference spectrum is interpreted as indicating an enzyme conformational change. No difference spectrum was observed with methylguanidine. 5. The ability of aliphatic alpha-l-amino acids to protect against inhibition by 5,5'-dithiobis-(2-nitrobenzoic acid) is proportional to the number of atoms in the carbon chain and inversely proportional to K(i). Ornithine gives greater protection than citrulline; analogues lacking the alpha-amino groups also protect. Agmatine, lacking the alpha-carboxy group, did not protect. 6. It is concluded that it is unlikely that the ;essential' thiol group in the enzyme interacts with any part of the arginine molecule during catalysis except, possibly, the alpha-carboxyl group.

Animals↗
PubMed1979

Inexpensive analog equipment for processing gas chromatography mass spectrometry data.

Using relatively simple analog circuitry, and an inexpensive analog frequency modulated tape recorder (or a modified audio recorder) for data storage, repetitively scanned spectra may be examined on an oscilloscope, and reconstructed mass chromatograms produced. The same equipment may be used for peak matching, and for selective ion detection over the full mass range of a sector instrument.

Chromatography, Gas↗
PubMed1979

Urinary dicarboxylic acids in patients receiving lithium or rubidium salts.

Lithium salts administered in therapeutic doses to four subjects who were kept on controlled diets increased up to fivefold the urinary output of some dicarboxylic acids. Some of the acids affected are intermediates in the tricarboxylic acid cycle, others are chemically similar but not directly related in metabolic terms. This is probably a direct effect on renal transport. Rubidium salts increased urinary 2-oxoglutarate output and blood 2-oxoglutarate levels, probably by some action on intermediary metabolism.

Bipolar Disorder↗
PubMed1978

Effects of rubidium chloride on the course of manic-depressive illness.

Clinical studies of the effects of rubidium ions on the course of manic-depressive illness are reported. It seems that rubidium tends to increase the length of manic phases and possibly reduces the extremes of mood. Rubidium did not seem to produce any severe side effects in the dose administered, but it has a long biological half-life and caution is still required. Some details of the CSF, RBC, saliva and plasma and urine kinetics are also reported.

Adult↗
PubMed1977

Lithium.

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Erythrocytes↗
PubMed1976

Determination of urinary monohydric and dihydric phenols by gas chromatography of the acetate and TMS derivatives. 4-Dimethylaminopyridine as a catalyst for acetylation reactions.

A procedure is described for the quantitative extraction of phenols from human urine. The compounds were chromatographed as the trimethylsilyl derivatives on wall-coated glass capillary columns. A more specific method of extraction involving the formation of acetate derivatives is also described. The acetates were prepared by treating dilute solutions of phenols at room temperature with acetic anhydride in the presence of 4-dimethylaminopyridine, which is a far more powerful catalyst than pyridine. Under these conditions N-acylamino acids are converted to azlactones.

4-Aminopyridine↗