Subject(s)
Antipsychotic Agents/therapeutic use , Dibenzothiazepines/therapeutic use , Drug Industry , Drug Utilization , Education, Medical, Continuing , Drug Utilization/statistics & numerical data , Drug Utilization/trends , Drug Utilization Review , Formularies, Hospital as Topic , Hospitals, Veterans , Humans , Minnesota , Practice Patterns, Physicians' , Quetiapine Fumarate , United StatesABSTRACT
We report on characterization of a 170,000 Da glycoprotein found exclusively in the PNS. We refer to this protein as the Schwann cell membrane glycoprotein (SAG). SAG contains the HNK-1 carbohydrate, which is considered by some to be a marker of adhesion molecules. Its N-terminal sequence is not similar to previously known polypeptide sequences. SAG is found exclusively in the PNS, is present in rat sciatic nerve prior to myelination, and is in both myelinating and nonmyelinating Schwann cells. Tumors of Schwann cell lineage express SAG where axons are present (neurofibromas) but do not in the absence of axons (schwannomas). Schwannoma cells in culture do not express SAG even when exposed to forskolin, an activator of adenylate cyclase. However, schwannoma cells grown in the presence of a neuronal cell line (PC12) express SAG.
Subject(s)
Membrane Glycoproteins/metabolism , Nerve Tissue Proteins/metabolism , Peripheral Nerves/metabolism , Schwann Cells/metabolism , Amino Acid Sequence , Animals , Blotting, Western , Carbohydrate Metabolism , Humans , Lectins , Membrane Glycoproteins/genetics , Molecular Sequence Data , Nerve Tissue Proteins/genetics , Rats , Rats, Inbred Lew , Staining and Labeling , Tissue DistributionABSTRACT
Experimental allergic neuritis (EAN) was studied in the SJL/J mouse and compared to EAN in the Lewis rat. The Lewis rat developed hind limb weakness and weight loss while the SJL/J mouse had no discernible clinical abnormalities. The SJL/J mouse, however, suffered subclinical damage to peripheral nerve (PN) myelin. Both species reproducibly developed electrophysiologic dysfunction of PN and histopathology confined to the peripheral nervous system (PNS). Understanding of autoimmune demyelination in the central nervous system was greatly enhanced by the development of experimental allergic encephalomyelitis in the SJL/J mouse. We believe that EAN in the SJL/J mouse could lead to a similar increase in our understanding of autoimmune demyelination in the PNS.
Subject(s)
Mice, Neurologic Mutants/physiology , Neuritis, Autoimmune, Experimental/physiopathology , Peripheral Nerves/physiopathology , Action Potentials , Acute Disease , Animals , Cattle , Central Nervous System/pathology , Female , Humans , Immunization, Passive , Male , Mice , Muscles/physiopathology , Myelin Sheath/metabolism , Neuritis, Autoimmune, Experimental/immunology , Neuritis, Autoimmune, Experimental/pathology , Peripheral Nerves/pathology , Rats , Rats, Inbred Lew , Tissue Extracts/immunologySubject(s)
Antigens, Bacterial/immunology , Autoimmune Diseases/etiology , Bacteria/immunology , Epitopes/immunology , Myasthenia Gravis/etiology , Receptors, Nicotinic/immunology , Antibodies, Monoclonal/immunology , Antibody Specificity , Autoantibodies/immunology , Autoimmune Diseases/immunology , Cross Reactions , Humans , Myasthenia Gravis/immunologyABSTRACT
There is substantial evidence that human serum contains antibodies to many autoantigens. For example, all healthy people have autoantibodies (immunoglobulin M) to some undefined brain antigens. In this study immunoblots and immunohistochemical staining were used to detect antibodies to neural tissues in serum samples from 200 healthy people and 200 patients with various neurological diseases. Ninety-nine percent of the 400 subjects had serum immunoglobulin M and 95 percent had immunoglobulin G that bound to a 200-kilodalton protein in homogenates of neural tissues. In most cases there were no antibodies to anything else in the homogenates. The 200-kilodalton protein was the heaviest of the neurofilament triplet proteins. These observations do not support a role for antibodies to the 200-kilodalton protein of neurofilaments in the pathogenesis of neurological diseases.
