Polysialylated neural cell adhesion molecule is involved in the neuroplasticity induced by axonal injury in the avian ciliary ganglion

We demonstrated previously in the quail ciliary ganglion, that the immunore activity for the neural cell adhesion molecule labeling the postsynaptic sp ecializations of intraganglionic synapses decreases when synaptic remodelin g is induced by crushing the postganglionic ciliary nerves. Here we show, i n the same experimental conditions, that the immunolabeling for its polysia lylated non-stabilizing isoform, which promotes cell plasticity, increases at these subcellular compartments. In control ganglia, poor immunolabeling for the polysialylated neural cell adhesion molecule was occasionally obser ved surrounding the soma of the ciliary neurons, in correspondence with the calyciform presynaptic ending and the perineuronal satellite cells sheath. At the electron microscope, several neuronal compartments, including some postsynaptic specializations, somatic spines and multivesicular bodies, wer e immunopositive. Three to six days after ciliary nerve crush, both the num ber of ciliary neurons labeled for the polysialylated neural cell adhesion molecule and the intensity of their immunolabeling increased markedly. Elec tron microscopy revealed that, in parallel to the injury-induced detachment of the preganglionic boutons, numerous postsynaptic specializations were f ound to be immunopositive. Twenty days later, when intraganglionic connecti ons were re-established, polysialylated neural cell adhesion molecule immun oreactivity was comparable to that observed in control ganglia. The increas e in immunolabeling also involved the other neuronal compartments mentioned above, the perineuronal satellite cells and the intercellular space betwee n these and the ciliary neurons. From these results we suggest that the switch, at the postsynaptic speciali zations, between the neural cell adhesion molecule and its polysialylated f orm may be among the molecular changes occurring in axotomized neurons lead ing to injury-induced synaptic remodeling. Moreover, from the increase in p olysialylated neural cell adhesion molecule immunolabeling, observed at the somatic spines and at the interface between neurons and perineuronal satel lite cells, we suggest that this molecule may be involved not only in synap tic remodeling, but also in other more general aspects of injury induced ne uronal plasticity. (C) 2001 IBRO. Published by Elsevier Science Ltd. All ri ghts reserved.