Effects of axotomy on the expression and ultrastructural localization of N-cadherin and neural cell adhesion molecule in the quail ciliary ganglion: an in vivo model of neuroplasticity

• Published in: Neuroscience Vol. 91; no. 2; pp. 707 - 722
• Main Authors: Squitti, R, De Stefano, M.E, Edgar, D, Toschi, G
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01-01-1999; Elsevier
• Subjects: adhesion molecules; Animals; axonal damage; Axotomy; Biological and medical sciences; Cadherins - genetics; Cadherins - metabolism; Ciliary Body - innervation; ciliary ganglion; Coturnix; Coturnix japonica; Development. Senescence. Regeneration. Transplantation; Fundamental and applied biological sciences. Psychology; Ganglia, Parasympathetic - cytology; Ganglia, Parasympathetic - physiology; Ganglia, Parasympathetic - ultrastructure; Gene Expression Regulation; immunocytochemistry; Models, Neurological; Nerve Crush; Nerve Regeneration; Neural Cell Adhesion Molecules - genetics; Neural Cell Adhesion Molecules - metabolism; Neuronal Plasticity; Reverse Transcriptase Polymerase Chain Reaction; RT–PCR; Synapses - physiology; Synapses - ultrastructure; synaptic plasticity; Time Factors; Transcription, Genetic; Vertebrates: nervous system and sense organs; ciliary ganglion; axonal damage; immunocytochemistry; RT–PCR; GAPDH, glyceraldehyde phosphate dehydrogenase; N-CAM, neural cell adhesion molecule; PB, phosphate buffer; adhesion molecules; PCR, polymerase chain reaction; RT, reverse transcriptase; synaptic plasticity; apCAM, Aplysia cell adhesion molecule; IR, immunoreactivity; Neural cell adhesion molecule; Cadherin; Quail; Gene expression; Ophthalmic ganglion; Vertebrata; Axotomy; Autonomic nervous system; Ultrastructure; Synaptic plasticity; Development; Aves; Localization; Parasympathetic nervous system
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/S0306-4522(98)00660-5

Postganglionic nerve crush of the avian ciliary ganglion induces detachment of preganglionic terminals from the soma of the injured ciliary neurons, followed by reattachment at about the same time that the postganglionic axons regenerate to their targets. In order to determine the role played by cell adhesion molecules in this response, we have studied injury-induced changes in the amount and distribution of N-cadherin and neural cell adhesion molecule, together with modifications in the expression of their messenger RNAs. Both N-cadherin and neural cell adhesion molecule immunoreactivities associated with postsynaptic specializations decreased between one and three days following postganglionic nerve crush, preceding the detachment of the preganglionic boutons. Immunoreactivities subsequently increased between 13 and 20
days, in parallel with restoration of synaptic contacts on the ganglion cells and the progressive reinnervation of the peripheral targets. In contrast to the rapid decrease in immunoreactivity, the messenger RNA levels of N-cadherin and neural cell adhesion molecule both increased after crush, and remained elevated throughout the 20-day period of the experiment.
These results are consistent with roles for N-cadherin and neural cell adhesion molecule in the maintenance of synaptic contacts. The rapid regulation of these proteins in injury-induced synaptic plasticity occurs at the post-transcriptional level, whereas longer term regulation associated with the re-establishment of synapses may be promoted by the increased levels of gene expression.