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C L Weill

Publications and source records attributed to C L Weill.

25 records · Page 2Linked to original sources
PubMed1982

cGMP accumulation by spinal cord neurons during the period of neuromuscular junction formation.

A 4--5-fold increase in cGMP levels in spinal cord neurons has been demonstrated in vitro and in vivo upon association with skeletal muscle. The increase on cGMP was temporally coincident with the onset of neuromuscular junction formation and independent of any concomitant change in cAMP. The response was specific for spinal cord neurons cocultured with skeletal muscle; glial cells could not be substituted for spinal cord neurons nor could fibroblasts be substituted for muscle cells. The response was not dependent upon action potential activity, synaptic transmission or muscle contractile activity. Muscle conditioned medium was found to produce the largest increase of cGMP in spinal cord neurons of 23-fold.

Animals↗
PubMed1980

Regulation of acetylcholinesterase appearance at neuromuscular junctions in vitro.

The appearance of acetylcholinesterase (AChE) at newly formed nerve-muscle synapses depends on synaptic transmission. Synapses form when cultures are grown in the presence of acetylcholine receptor antagonists, but AChE does not accumulate at these synapses. The important component of transmission seems to be muscle activity. Treatment with dibutyryl cyclic GMP mimics muscle activity, directly inducing synaptic AChE appearance.

Acetylcholinesterase↗
PubMedDate not supplied

Prevention of natural motoneurone cell death by dibutyryl cyclic GMP.

Natural neuronal cell death is a well-described developmental phenomenon common to many nerve centres in a variety of animal species. Neuronal survival has been shown to depend on the presence and size of the available target tissue and it has been suggested that neuronal survival is dependent on successful competition for either a limited number of synaptic sites or a limited amount of trophic factor(s). In the lateral motor column of the lumbar spinal cord in the chick embryo, the period of axon elongation and innervation of the periphery has been shown to precede that of natural motoneurone cell death. While muscle contractile activity appears to regulate the extent of motoneurone death, to date the intracellular molecular events that initiate and regulate the developmental process of natural neuronal cell death or, more importantly, neuronal survival are unknown. Our earlier studies suggested that either contact or association between spinal cord processes and muscle cells during neuromuscular junction formation in vivo leads to an increase in cyclic GMP in whole spinal cord. We now show that treatment of chick embryos with the membrane-permeable cyclic GMP analogue, dibutyryl cyclic GMP during the period of natural motoneurone cell death prevents greater than 58% of natural motoneurone cell death in the lumbar lateral motor column.

Animals↗