PMID- 9294861
OWN - NLM
STAT- MEDLINE
DCOM- 19971016
LR  - 20181201
IS  - 0893-7648 (Print)
IS  - 0893-7648 (Linking)
VI  - 14
IP  - 3
DP  - 1997 Jun
TI  - Intercellular communication that mediates formation of the neuromuscular 
      junction.
PG  - 143-70
AB  - Reciprocal signals between the motor axon and myofiber induce structural and 
      functional differentiation in the developing neuromuscular junction (NMJ). 
      Elevation of presynaptic acetylcholine (ACh) release on nerve-muscle contact and 
      the correlated increase in axonal-free calcium are triggered by unidentified 
      membrane molecules. Restriction of axon growth to the developing NMJ and 
      formation of active zones for ACh release in the presynaptic terminal may be 
      induced by molecules in the synaptic basal lamina, such as S-laminin, heparin 
      binding growth factors, and agrin. Acetylcholine receptor (AChR) synthesis by 
      muscle cells may be increased by calcitonin gene-related peptide (CGRP), ascorbic 
      acid, and AChR-inducing activity (ARIA)/heregulin, which is the best-established 
      regulator. Heparin binding growth factors, proteases, adhesion molecules, and 
      agrin all may be involved in the induction of AChR redistribution to form 
      postsynaptic-like aggregates. However, the strongest case has been made for 
      agrin's involvement. "Knockout" experiments have implicated agrin as a primary 
      anterograde signal for postsynaptic differentiation and muscle-specific kinase 
      (MuSK), as a putative agrin receptor. It is likely that both presynaptic and 
      postsynaptic differentiation are induced by multiple molecular signals. Future 
      research should reveal the physiological roles of different molecules, their 
      interactions, and the identity of other molecular participants.
FAU - Daniels, M P
AU  - Daniels MP
AD  - Laboratory of Biochemical Genetics, National Heart, Lung and Blood Institute, 
      National Institute of Health, Bethesda, MD 20892, USA.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Mol Neurobiol
JT  - Molecular neurobiology
JID - 8900963
RN  - 0 (Receptors, Cholinergic)
RN  - JHB2QIZ69Z (Calcitonin Gene-Related Peptide)
RN  - PQ6CK8PD0R (Ascorbic Acid)
SB  - IM
MH  - Animals
MH  - Ascorbic Acid/metabolism
MH  - Calcitonin Gene-Related Peptide/physiology
MH  - Cell Communication/*physiology
MH  - Genetic Techniques
MH  - Humans
MH  - Models, Biological
MH  - Muscle Fibers, Skeletal/physiology
MH  - Neuromuscular Junction/*physiology
MH  - Neurons/physiology
MH  - Receptors, Cholinergic/biosynthesis/*physiology
MH  - Signal Transduction
MH  - Synapses/*physiology
RF  - 225
EDAT- 1997/06/01 00:00
MHDA- 1997/09/19 00:01
CRDT- 1997/06/01 00:00
PHST- 1997/06/01 00:00 [pubmed]
PHST- 1997/09/19 00:01 [medline]
PHST- 1997/06/01 00:00 [entrez]
AID - 10.1007/BF02740654 [doi]
PST - ppublish
SO  - Mol Neurobiol. 1997 Jun;14(3):143-70. doi: 10.1007/BF02740654.