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Biomedical subjects

N Miani

Publications and source records attributed to N Miani.

8 recordsLinked to original sources
PubMed1979

Appearance of new alpha-bungarotoxin-acetylcholine receptors in cultured sympathetic ganglia of chick embryos.

alpha-Bungarotoxin (alpha-BuTX) has been used as a marker for studying the production of alpha-bungarotoxin-acetylcholine receptors (alpha-BuTX-AChRs) in explants of chick embryo sympathetic ganglia cultured in vitro. New alpha-BuTX-AChRs appear rapidly in the explants after blocking of the pre-existent ones with the toxin (40% of the total receptors at 3 h). There is a portion of alpha-BuTX-AChRs in the explants which for a short time is not accessible to the toxin. This portion constitutes the precursor pool of receptors and represents 18% of the total. The precursor pool of receptors supplies the neurons with new receptors for 1-2 h in the absence of protein synthesis. The appearance of new receptors from the precursor pool is an energy-dependent process.

Acetylcholine↗
PubMed1978

alpha-Bungarotoxin-acetylcholine receptors in the chick ciliary ganglion: effects of deafferentation and axotomy.

alpha-Bungarotoxin (alpha-BuTX) binds in a saturable and practically irreversible fashion to membrane-associated receptors in the ciliary ganglion of the adult chick. The binding of toxin to receptors is competitively inhibited by nicotinic cholinergic ligands, and for these properties the receptors are regarded as acetylcholine receptors of the nicotinic type (alpha-buTX-AChRs). The rate constant of association (K1) and dissociation (K-1) of the toxin-receptor reaction has been estimated to be K1 = 7.4 x 104 M(-1) sec(-1) and K-1 = 9.6 X 10(-6) sec(-1), respectively. Light autoradiography shows that most, if not all, the receptors are related to surface membrane, probably to synaptic areas of both choroid and ciliary neurons. The choroid neurons contain more receptors than the ciliary ones. A single chick ciliary ganglion binds specifically 47 fmole of alpha-BuTX in situ corresponding to 2.83 x 1010 alpha-BuTX-AChRs/ganglion. No changes in number and distribution of the toxin receptors occur following preganglionic denervation. Conversely, postganglionic axotomy causes a rapid disappearance of the receptors in situ. Since binding experiments in vitro revealed a partial, instead of a total, loss of the receptors, it is suggested that the disappearance of the receptors in situ includes both a partial loss of the original receptors and the masking of the residual ones.

Acetylcholine↗
PubMed1975

Soluble and membrane-bound S-100 protein in cerebral cortex synaptosomes. Properties of the S-100 receptor.

Within cerebral cortex synaptosomes, S-100 protein can be recovered in two forms: soluble and membrane-bound. Synaptosomal S-100 is mainly a soluble protein (85 percent). The membrane-bound S-100 is differently distributed in the synaptosomal membranes, intraterminal mitochondria, and synaptic vesicles. S-100 binds to a specific receptor. The binding is time-dependent, reversible and saturable with respect to S-100. The number of receptors is calculated to be about 9 times 10(12)/mg protein, since saturation is achieved at 31 ng [125I]S-100/0.1 mg protein of disrupted synaptosomes. The rate constant for association of S-100 with its receptor at 37 degrees C, k1, is 4.74 times 10(4) M(-1) sec(-1), and the rate constant for dissociation, k-1, 9.24 times 10(-4) sec(-1).

Animals↗
PubMed1975

Concanavalin A as a probe for studying the mechanism of metabolic stimulation of leukocytes.

The disruption of the molecular organization of the plasma membrane of leukocytes by phagocytosable particles, or by agents such as surfactants, antibodies, phospholipase C, fatty acids and chemotactic factors, leads to a stimulation of the phagocyte oxidative metabolism. Concanavalin A (Con A) has been used as a tool to study the mechanism of this metabolic regulation. The binding of Con A to the surface of polymorphonuclear leukocytes (PMNL) or macrophages produces a rapid enhancement of oxygen uptake and glucose oxidation through the hexose monophosphate pathway (HMP). This is explained by an activation of the granular NADPH oxidase, the key enzyme in the metabolic stimulation. The effect of Con A is not due to endocytosed lectin, since Con A covalently coupled to large sepharose beads still acts as stimulant. The metabolic changes caused by Con A are reversible. If, after the onset of stimulation, sugars with high affinity for Con A are added to the leukocyte suspension, the activity of granular NADPH oxidase and the rate of respiration and glucose oxidation return to their resting values. The metabolic burst, while partially supressed by treatment of PMNL with iodoacetate, sodium flouride and cytochalasin B, is slightly increased by colchicine. Con A induces a selective release of granular enzymes (beta-glucuronidase, peroxidase, alkaline phosphatase) from PMNL, whereas no leakage of cytoplasmic enzymes is observed. The enzyme release is inhibited by iodoacetate and by drugs known to increase cell levels of cyclic AMP. Based on a current view of the mode of interaction between Con A and cell surfaces, a model of the metabolic disruption of leukocytes is presented.

Animals↗