Denervation of newborn rat muscle does not block the appearance of adult fast myosin heavy chain.

Several observations, both in vivo and in vitro, have indicated that the development and maturation of mammalian skeletal muscle fibres is influenced by nerve-muscle interactions. Morphological maturation of newly regenerated adult mouse muscle fibers in an organotypic nerve-muscle culture system depends on the presence of spinal cord neurones. Sciatic nerve transection in newborn rats has been shown to modify the development of the histochemical and contractile properties of the denervated muscles. In addition, neural influences are important for the appearance of certain of the myosin small subunits. It has been proposed that the nerve also controls the changes in myosin heavy chain isozymes appearing during development. One such transition occurs in rat muscle where the neonatal form of myosin heavy chain is replaced by the adult form during the second post-natal week. Here we demonstrate that innervation of the rat gastrocnemius muscle (a fast-contracting muscle in the adult) is not required for the appearance of the adult form of myosin heavy chain.

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. The inhibition is due to partial phospholipid hydrolysis leading to inactivation of membrane-bound receptor. (2) Bee venom phospholipase A2 together with the synergistically acting peptide, melittin, causes receptor solubilization up to 80% of preformed receptor-ligand complex can be solubilized in this manner. (3) Lysophosphatidylcholine, a product of phospholipid hydrolysis, solubilizes performed receptor-ligand complex to a similar extent. Several other detergents were tested for their ability to solubilize receptor-ligand complex. Digitonin appears to be most effective in solubilizing such a complex.

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. Antibodies against both non-toxin and ligand binding sites were measured in IgG subclasses. Most of the antibodies of the first type belonged to either subclass 1 or 3. They were, however, never absent from subclasses 2 and 4. Antibodies of the second type were not found in subclasses 2 and 4 except in one case. In 3 cases they were present exclusively in subclass 3. In 3 patients there was no correlation between the subclass distribution of the antibodies for the different binding sites.

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.

[Antibodies against nicotine-like acetylcholine receptors of central nervous system and muscles in epileptics with IgA deficiency]. / Antikörper gegen nicotinartige Acetylcholinrezeptoren des Zentralnervensystems und der Muskulatur bei Epileptikern mit IgA-Mangel.

Anti-muscle nicotinic acetylcholine receptor (nAR) antibodies were sought in epileptic patients without clinical signs of myasthenia gravis. Low titers of such antibodies were found in 3 cases characterized by primary generalized seizures, IgA deficiency and HLA A1 and B8 antigens. These three patients also had anti-brain nAR antibodies. In the serum of one patient with myasthenia gravis, anti-brain nAR antibodies were also detected. The titer was low despite a high titer of anti-muscle nAR antibodies. This may reflect the fact that the immune reaction in the three epileptic patients is primarily directed against the brain nAR.