Galanin expression in sympathetic ganglia after partial axotomy is highly localized to those neurons that are axotomized

The neuropeptide phenotype of adult sympathetic neurons changes dramatically after postganglionic nerve transection. Studies, thus far, have been done on the superior cervical ganglion; however, one limitation of this preparation is that it is necessary to transect the postganglionic axons quite close to the ganglion. In the present study, we examined the effects of axonal damage on galanin-like immunoreactivity in the middle and inferior cervical ganglion complex. With these ganglia, it is possible to transect postganglionic axons at a considerable distance from their cell bodies and, therefore, to examine the extent to which local tissue damage, rather than specific axonal transection, is required for these changes in neuropeptide phenotype to occur. The anatomy of this system also allowed us to determine the extent to which the changes in galanin expression are restricted to those neurons that have been axotomized. The axons of a small population of the neurons in the middle and inferior cervical ganglia complex project into the cervical sympathetic trunk. Within two days after this trunk was transected, there was an increase in the level of galanin-like immunoreactivity in the complex and in the number of immunostained principal neurons. These neurons were concentrated primarily in the most rostral part of the complex. An increase in galanin-like immunoreactivity also occurred in response to the systemic administration of the sympathetic neurotoxin 6-hydroxydopamine. In that case, many more neurons were affected than after transection of the cervical sympathetic trunk, and the neurons were distributed evenly throughout the ganglion complex. After the cervical sympathetic trunk was cut, the cell bodies of the axotomized neurons were identified by retrograde labeling from the point of transection with Fast Blue. The vast majority (86%) of neurons that exhibited galanin-like immunoreactivity were labeled with Fast Blue, indicating that the changes in peptide expression occur primarily, and perhaps exclusively, in axotomized neurons. Forty-two per cent of the Fast Blue-labeled neurons exhibited galanin-like immunoreactivity, suggesting that sympathetic neurons within a ganglion do not behave as a homogenous population in response to axotomy. The results also indicate that tissue damage in the vicinity of a ganglion is not a necessary triggering stimulus for this change in neuropeptide phenotype. The data are consistent with the hypothesis that a specific l