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Biomedical subjects

B Collier

Publications and source records attributed to B Collier.

At least 109 records · Page 6Linked to original sources
PubMed1982

Studies on presynaptic cholinergic mechanisms using analogues of choline and acetate.

Experiments in which analogues of choline and acetate were used in an attempt to elucidate presynaptic cholinergic mechanisms are described. The stimulation-induced accumulation of choline analogues in a sympathetic ganglion was used as an indicator of choline transport activation and the effects of various conditions on this phenomenon were tested. Acetylcholine synthesis and release, in the presence of choline, were then measured under similar conditions in order to explore the relationship between choline uptake and acetylcholine synthesis. Finally, the synthesis, storage and release of analogues of acetylcholine with altered acetyl moieties, propionylcholine and butyrylcholine, were studied using the Torpedo electric organ. Both of these analogues were incorporated into synaptic vesicles, but while butyrylcholine was as releasable as acetylcholine, propionylcholine was less releasable.

Acetates↗
PubMed1981

A critical evaluation of the use of toxins from Dendroaspis viridis to block nicotinic responses at central and ganglionic synapses.

Previous work by other investigators has shown that toxins prepared from Dendroaspis viridis venom block cholinergic transmission at the neuromuscular junction, as well as nicotinic transmission in frog spinal cord and in snail neurons. This suggested that these ligands may be useful for studying nicotinic receptors in the central nervous system. Thus, Dendroaspis viridis venom was fractionated into its toxin components. Only one of the fractions possessed activity as assessed by: (1) inhibition of alpha-bungarotoxin (alpha-BGT) binding at the neuromuscular junction (25% at 50 microgram toxin/ml) or (2) inhibition of the ventral root--dorsal root potential (VR--DRP), a nicotinic response in frog spinal cord. However, in the spinal cord preparation, in addition ot this blockade of the nicotinic pathway, convulsant activity and an increase in the amplitude of other root potentials was observed. Binding experiments using [125I]dendrotoxin demonstrated that the labeled compound bound to central nervous tissue such as brain or spinal cord; this was not displaced by nicotine (10(-4) M) or D-tubocurarine (10 (-4) M), a nicotinic antagonist, indicating either non-specific binding or binding to a non-nicotinic receptor. These results thus suggest that toxins from Dendroaspis viridis venom are not suitable ligands for central nicotinic receptors. In addition, as experiments also demonstrated that the dendrotoxins did not block cholinergic transmission in frog sympathetic ganglia, it contraindicates their use at ganglionic nicotinic receptors.

Acetylcholine↗
PubMed1981

Effect of choline on central dopaminergic function in normal subjects.

Oral administration of choline (10 g) had no effect on basal serum growth hormone or prolactin concentrations in normal subjects (N = 5). Choline significantly enhanced the increase in growth hormone secretion induced by apomorphine HCl (0.5 mg s.c.). These data suggest that cholinergic mechanisms may enhance hypothalamic-pituitary dopaminergic function in man in contrast to their inhibitory effect on dopaminergic function in the basal ganglia.

Adult↗
PubMed1981

Effect of increasing choline, in vivo and in vitro, on the synthesis of acetylcholine in a sympathetic ganglion.

The experiments described in this paper were designed to test whether increasing choline availability over normal physiological levels increases acetylcholine synthesis in the cat's superior cervical ganglion. When ganglia were perfused with Krebs solution, an increase in the medium's choline concentration over physiological (10(-5)M) levels increased tissue choline but did not increase tissue acetylcholine or the release of acetylcholine from stimulated ganglia. However, increasing plasma choline in the whole animal increased ganglionic acetylcholine levels. The basis for this difference in the effects of in vivo and in vitro exposure to elevated choline levels on the tissue acetylcholine content was found to involve plasma factor(s), rather than indirect actions of choline, and the acetylcholine content of isolated ganglia was increased when the tissue was perfused with plasma, instead of Krebs solution, containing 10(-3)M-choline. The extra acetylcholine generated by this procedure was associated with a subsequent transient increase in transmitter release during short intervals of stimulation, but most of the extra acetylcholine was not readily available for release from stimulated ganglia. It is concluded that increasing choline available to sympathetic ganglia over physiological concentration does not have a sustained effect on the turnover of releasable transmitter under the conditions of these experiments.

Acetylcholine↗
PubMed1981

The structural specificity of choline transport into cholinergic nerve terminals.

The accumulation of choline, homocholine, and 4-hydroxybutyltrimethylammonium by rat brain synaptosomes was measured; the choline uptake mechanism transported homocholine but not hydroxybutyltrimethylammonium, which, in addition, did not block choline accumulation. In cats' superior cervical ganglia, preganglionic nerve stimulation increased the accumulation of homocholine, but not that of hydroxybutyltrimethylammonium. It is concluded that the substrate specificity of the choline transport mechanism is such that increasing the N--O atom distance by one methylene group retains affinity, but increasing this distance by two methylene groups does not.

Animals↗
PubMed1981

Convulsant and possible anticholinergic actions of dendrotoxin in the amphibian spinal cord.

1 Dendrotoxin (DTOX)6, 6a and 5,6-1, fractions of the venom isolated from the green mamba (Dendroaspis viridis) promoted both spontaneous and stimulus-coupled rhythmic activity and antagonized the cholinergically mediated ventral root-dorsal root potential (VR-DRP) of frog spinal cord. The different time course and reversibility of these two effects indicates that the toxin has two entirely separate sites of action on the frog spinal cord. 2 Since DTOX 6 neither blocked nor enhanced responses of ventral and dorsal roots to glutamate, gamma-aminobutyric acid (GABA), beta-alanine, glycine or aspartate, it is unlikely that its convulsant action resulted from an alteration of the postsynaptic actions of inhibitory or excitatory amino acids. 3 An alteration in the threshold for action potential generation could perhaps contribute to the convulsant action of DTOX 6, although other mechanisms such as blockade of the release of unspecified inhibitory substances cannot be excluded. 4 In addition to the lack of effect on amino acid responses, DTOX failed to block the polysynaptic DR-VRP or DR-DRP pathways, which are mediated at least in part by amino acid neurotransmitters. Although this would be consistent with a specific action of DTOX at the cholinergic synapse of the VR-DRP pathway, this site of action has not yet been demonstrated unequivocally. Other possible mechanisms whereby DTOX could block VR-DRP are discussed.

Animals↗
PubMed1981

Alzheimer disease: lack of effect of lecithin treatment for 3 months.

Eleven outpatients with Alzheimer disease of moderate severity completed a double-blind placebo-controlled crossover trial of lecithin. Each patient received 10 gm three times daily of a placebo for 3 months. Plasma choline levels rose threefold and remained at that level throughout the lecithin administration period. A significant difference between mean baseline scores and treatment scores was found on tests of new learning ability, indicating a practice effect in these tests. However, there were no differences between mean placebo and lecithin scores on any of the psychological test measures.

Aged↗
PubMed1980

N-Ethyl analogues of choline as precursors to cholinergic false transmitters.

Cat superior cervical ganglia perfused with the choline analogue, diethylcholine, acetylated the analogue and acetyldiethylcholine was subsequently released from the ganglia in response to preganglionic nerve stimulation by a Ca2+-dependent mechanism. Rat cerebral cortical slices incubated with monoethylcholine or diethylcholine acetylated the choline analogues, and both acetylmonoethylcholine and acetyldiethylcholine were released from the slices in response to stimulation by a high K+ concentration. In brain slices pre-incubated with monoethylcholine, diethylcholine, or triethylcholine, acetylated derivatives of the choline analogues were found in both free and bound nerve-ending stores, similar to the subcellular localization of [3H]acetylcholine (ACh) in brain slices pre-incubated with [3H]choline; the relative distribution of each of the acetylated choline analogues between the two nerve-ending stores differed only slightly from that of [3H]ACh. Nerve-ending free and bound stores of acetyldiethylcholine were equally depleted when brain slices were stimulated under conditions that cause depletion of releasable acetyldiethylcholine stores; similar results were obtained with acetyltriethylcholine. It is concluded that the three acetylated ethyl analogues of choline fulfill the necessary criteria for identification as cholinergic false transmitters, and that, under the conditions of the present experiments with brain, the false transmitters are able to distribute similarly to ACh between nerve-ending stores.

Acetylation↗