The neurons in the superior cervical ganglion are active in plasticity and re-modelling in order to adapt to requirements. However, so far, only a few studies dealing with synaptic vesicle related proteins during adaptive processes have been published. In the present paper, changes in content and expression of the synaptic vesicle related proteins in the neurons after decentralization (cutting the cervical sympathetic trunk) or axotomy (cutting the internal and external carotid nerves) were studied. Immunofluorescence studies were carried out using antibodies and antisera against integral membrane proteins, vesicle associated proteins, NPY, and the enzymes TH and PNMT. For colocalization studies, the sections were simultaneously double labelled. Confocal laser scanning microscopy was used for colocalization studies as well as for semi-quantification analysis, using the computer software. Westen blot analysis, in situ 3′-end DNA labelling, and in situ hybridization were also employed. After decentralization of the ganglia several of the synaptic vesicle proteins (synaptotagmin I, synaptophysin, SNAP-25, CLC and GAP-43) were increased in the iris nerve terminal network, but with different time patterns, while TH-immunoreactivity had clearly decreased. In the ganglia, these proteins had decreased at 1 day after decentralization, probably due to degeneration of the pre-ganglionic nerve fibres and terminals. At later intervals, these proteins, except SNAP-25, had increased in the nerve fibre bundles and re-appeared in nerve fibres outlining the principal neurons. Immunoblot results confirmed the immunocytochemical observations. In situ hybridization showed that the increase of GAP-43 protein (a protein actively involved in neuronal plasticity) was parallelled by an increase in GAP-43mRNA, indicating up-regulation at the transcriptional level. After axonal injury not only the neurons, but also the satellite cells, reacted. Many neurons and satellite cells in the cranial part of the ganglia disappeared after axotomy. Using the in situ 3′-end DNA labelling method, evidence for apoptosis as the mechanism for this cell death was obtained. Neurons in the middle and caudal parts of the ganglia, which normally show undetectable levels of GAP-43 and galanin, showed increases of GAP-43 protein, GAP-43mRNA and galanin, accompanied by decreases in TH and VMAT2. The results suggest that the neurons had switched from neurotransmission to regeneration/plasticity. Conclusion: Many of the major synaptic vesicle proteins showed pronounced alterations following decentralization or axotomy, and are possibly participating in reorganization and remodelling reactions after trauma. The preganglionic innervation of the SCG probably participates in the regulation of GAP-43 as well as of SNAP-25, both suggested to be involved in neuronal regeneration, but the mechanisms appear to be different. Neurons as well as satellite cells near the lesion reacted to axotomy of the major post-ganglionic nerves. While many cells in the cranial part of the ganglion showed apoptosis, the surviving neurons in the middle and caudal parts showed clear signs of regeneration/plasticity.
