Selective solubilization by melittin of glycophorin A and acetylcholinesterase from human erythrocyte ghosts.

Melittin, the main basic and hydrophobic peptide of bee venom, has been used for solubilizing membrane components of the human erythrocyte ghost. Up to 1.0 mM, it does not extract any phospholipid.

Receptor-like activity of a monoclonal anti-idiotypic antibody against an anti-acetylcholine receptor antibody.

A monoclonal anti-idiotypic antibody against an anti-acetylcholine receptor antibody from a patient with myasthenia gravis was shown to bind the cholinergic ligand alpha-bungarotoxin. This binding could be inhibited by other cholinergic ligands, both antagonists and agonists. The anti-idiotype was also able to elicit the production of anti-receptor antibodies in mice.

Lack of cross-reactivity of a monoclonal antibody against the neurotransmitter site of Torpedo nicotinic acetylcholine receptor with muscle receptors from several sources.

A monoclonal antibody raised against Torpedo nicotinic acetylcholine receptor has been used to study the neurotransmitter binding site of the acetylcholine receptor from several sources. When tested on Torpedo receptor, this monoclonal antibody inhibited binding of alpha-bungarotoxin to 50% of the available sites. The failure to completely inhibit binding of the toxin is attributed to the orientation of the determinant for the monoclonal antibody on the receptor molecule.

Evidence for sialic acid on the nicotinic acetylcholine receptor from Torpedo marmorata.

The nicotinic acetylcholine receptor from Torpedo marmorata was treated with neuraminidase. Direct determination of sialic acid released gave about 1 mole sialic acid per mole receptor. Lectin binding studies of the sugars accessible on the receptor molecule were performed after sialic acid hydrolysis.

Reconstitution of pure acetylcholine receptor in phospholipid vesicles and comparison with receptor-rich membranes by the use of a potentiometric dye.

Acetylcholine receptor, isolated in Triton X-100 on a cobra alpha-neurotoxin affinity column was incorporated into unilamellar phospholipid vesicles by a detergent depletion method using Amberlite XAD-2. Vesicles of an average diameter of 25 nm were formed, as verified by freeze-fracture electron microscopy and gel filtration. 85 to 95% of the alpha-bungarotoxin binding sites of the reconstituted acetylcholine receptor were oriented towards the outside of the vesicles.

Encephalopathy, peripheral neuropathy, dysautonomia, myasthenia gravis, malignant thymoma, and antiacetylcholine receptor antibodies in the CSF.

A 54-year-old man suffered from multiple neurologic disturbances (polyneuropathy, encephalopathy, dysautonomia) associated with myasthenia gravis and malignant thymoma. No morphological signs of inflammation were present in the brain and peripheral nerves. Antiacetylcholine receptor antibodies were present in the brain and peripheral nerves.

Specific binding to isolated acetylcholine receptor of a synthetic peptide duplicating the sequence of the presumed active center of a lethal toxin from snake venom.

To verify the existence of a lethal "active center" in snake venom neurotoxins and to assess its delineation within their polypeptide sequences, a tritriacontapeptide matching residues 16-48 of the natural "major" toxin of Naja naja philippinensis (Hauert, J., Maire, M., Sussmann, A.

Inactivation and solubilization of opiate receptors by phospholipases A2.

(1) As previously shown, stereospecific binding of opiates to membrane bound receptors is inhibited by treatment with small amounts of phospholipase A2 from Vipera russelli. This effect is quantified and compared with the enzymes from the venoms of Naja Naja siamensis, Apis Mellifica and from porcine pancreas. All enzymes are equally effective.

Monoclonal anti-torpedo receptor antibodies used to study antibody heterogeneity in myasthenic sera.

Monoclonal antibodies against Torpedo acetylcholine receptor were used to define the binding regions of cross-reacting, anti-receptor antibodies from sera of myasthenic patients. Cross-reacting antibodies were directed mainly against the toxin-binding region of the receptor and a region remote from the acetylcholine-binding site. Few patients had antibodies against the acetylcholine-binding site region.

Binding properties and subclass distribution of anti-acetylcholine receptor antibodies in myasthenia gravis.

Acetylcholine receptor antibodies were studied in the serum of 21 myasthenic patients. In 18 cases antibodies directed against sites other than the toxin binding were present whereas in 10 cases only there was a measurable inhibition of the ligand binding site. These 10 sera were from the 6 patients in stage IIB, III and IV and from 4 of the 12 patients in stage IIA.

Purification and chemical characterization of melittin and acetylated derivatives.

Melittin, the main basic and hydrophobic peptide of bee venom, displays marked detergent-like properties. At high peptide concentration, and depending on salt and pH, it forms a tetramer. This is prevented by using urea.

Characterization of iodinated derivatives of alpha-bungarotoxin.

The iodination of alpha-bungarotoxin and the reactivity of iodinated derivatives towards nicotinic acetylcholine receptor are described. 125I2- and 125I-alpha-bungarotoxin can be resolved, but the latter was not separated from unreacted alpha-bungarotoxin. A study of the reactivities of the various forms of the toxin towards nicotinic acetylcholine receptor indicated that di-iodination had modified its reactivity.

A form of acute experimental autoimmune myasthenia gravis in mice occurring in absence of detectable circulating anti-acetylcholine receptor antibodies. Acute experimental myasthenia in mice.

A form of acute experimental autoimmune myasthenia gravis (EAMG) appears within 10 days after immunization of mice with rat acetylcholine receptor (AcChR) in complete adjuvant. This acute phase of EAMG differs from the chronic form reported earlier in the absence of detectable circulating anti-AcChR antibodies and by electrophysiologic signs of neuromuscular blockade which are not reversed by edrophonium injection. This form of acute EAMG occurs similarly in animals whose humoral response has been markedly reduced by pretreatment with cyclophosphamide.

Antibodies from myasthenic patients that compete with cholinergic agents for binding to nicotinic receptors.

We have purified immunoglobulins from sera of myasthenic patients and have identified antibodies directed against the cholinergic ligand-binding site of the nicotinic acetylcholine receptor. In the serum of one patient analyzed in detail these antibodies belonged to the IgG3 class, and their effects were as follows: (i) In chicken embryo myogenic cultures, antibody binding was both competitive with 125I-labeled alpha-bungarotoxin and irreversible on a time scale of hours. (ii) 125I-Labeled alpha-bungarotoxin was not displaced by antibody from preformed complexes and, conversely, antibody was not displaced by toxin.

Antibodies to acetylcholine receptor in patients with thymoma but without myasthenia gravis.

Antibodies to acetylcholine receptor were found in 3 of 11 patients with a thymoma removed by operation but without myasthenia gravis. Because masthenia gravis may appear after removal of the thymoma, detection of antiacetylcholine receptor antibodies may have predictive value.

[Clinical and immunological studies on a patient with myasthenia gravis before and after repeated plasma exchange].

A 56-year-old patient with severe acquired myasthenia gravis refractory to conventional therapy underwent a series of plasma exchanges. Three single exchanges did not improve her status. A series of intensive plasma exchanges of 6 liters each on 4 consecutive days reduced her anti-acetylcholine receptor antibodies to one-tenth of the initial value.

[Clinical and biological evolution of myasthenia gravis after thymectomy in a 13-year-old girl].

A 13-year-old girl suffering from rhumatoid arthritis developed a myasthenia gravis. Her circulating anti-acetylcholine receptor antibodies were observed before and after thymectomy. Surgical removal of the thymus was followed by complete clinical remission associated with a progressive decrease of the antibody level; these antibodies did not disappear completely even as late as 2 years after the operation.