19 research outputs found
Neuronal cell adhesion molecules and cytotactin are colocalized at the node of Ranvier.
The motor innervation of skeletal muscles in the motor end-plate disease mutant mouse (med and medj alleles).
Synapse formation in heterologous co-cultures of rat spinal cord dissociated neurons and mouse myotubes from trypsin-dissociated, post-natal muscles.
Intense ultraterminal sprouting from motor nerves and ultrastructural aspects of the neuromuscular junction and non-junctional sarcolemma of the soleus (slow-twitch) muscle in motor endplate disease in the mouse.
Extensive nerve overgrowth and paucity of the tailed asymmetric form (16 s) of acetylcholinesterase in the developing skeletal neuromuscular system of the dysgenic (mdg/mdg) mouse.
Impairment of T lymphocyte functions in mice with motor end-plate disease.
The present paper reports complex immunological anomalies associated with motor end-plate disease (Med) in mice. Motor end-plate disease is a severe neuromuscular disorder which leads to death (around the 25th of life) in the Medj/Medj mutant, while the heterozygotes quickly recover from mild manifestations. Medj/Medj and Medj/ + mice share some of the immunological aberrations: reduced PFC response to SRBC in 14-16 day old mice, with reduced suppressor cell function and precocious maturation of the cytotoxic response to allogeneic cells in 21-23 day old mice. The diminished PFC response is corrected in adult Medj/ + mice but persists in the small group of Medj/Medj which escape death and which were studied between the 6th and 16th week of life. In addition, the thymus and spleen of Medj/Medj mice are greatly reduced in size, a symptom which appears with the onset of the clinical disease. Also, a reduction in the NK activity in the small group of older, surviving mice was noted. T and B lymphocyte proportions and the proliferative responses to T cell mitogens were not impaired in 14-16 day old mice. The role of these abnormalities in the pathogenesis of the disease is not known. Since some of these anomalies are shared by Medj/Medj and Medj/ +, the latter of which present no or mild and transient neurological manifestations, there is no clear link between the immunological and neuromuscular disorders