CHANGES IN THE MACROPHAGE POPULATION OF THE RAT SUPERIOR CERVICAL-GANGLION AFTER POSTGANGLIONIC NERVE INJURY

Citation
Rc. Schreiber et al., CHANGES IN THE MACROPHAGE POPULATION OF THE RAT SUPERIOR CERVICAL-GANGLION AFTER POSTGANGLIONIC NERVE INJURY, Journal of neurobiology, 27(2), 1995, pp. 141-153
Citations number
71
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00223034
Volume
27
Issue
2
Year of publication
1995
Pages
141 - 153
Database
ISI
SICI code
0022-3034(1995)27:2<141:CITMPO>2.0.ZU;2-T
Abstract
Following peripheral nerve transection, a series of biochemical change s occurs in axons and Schwann cells both at the site of the lesion and distal to it. Macrophages differentiated from monocytes that invade t he area in response to transection (elicited macrophages) and, perhaps , also macrophages normally present in the tissue (resident macrophage s) play important roles in these changes. In addition, nerve transecti on produces changes in the cell bodies of axotomized neurons and their surrounding glial cells, located at some distance from the lesion. To determine whether macrophages might play a role in the changes occurr ing in the superior cervical ganglion (SCG) after axotomy, we examined the presence of macrophages before and after axonal damage. The monoc lonal antibodies ED1, ED2, and OX6 were used, each of which recognizes a somewhat different population of macrophages. Ganglia from normal r ats contained a population of resident cells that were ED2+ but very f ew that were ED1+. Within 2 days after the postganglionic nerves were transected, the number of ED1+ cells increased substantially, with lit tle change in immunostaining for ED2. These data, in combination with published studies on other tissues, suggest that ED1 in the SCG is sel ective for elicited macrophages and ED2 for resident macrophages. OX6 immunostaining was prominent in normal ganglia but also increased sign ificantly after axotomy, suggesting that it reflects both macrophage p opulations. Systemic administration of 6-hydroxydopamine, a neurotoxin that causes the destruction of sympathetic nerve endings, also produc ed an increase in ED1 immunostaining. Thus, the change in ED1 immunost aining in the SCG does not require surgery, with the attendant severin g of local blood vessels and connective tissue, but rather only the di sconnection of sympathetic neurons from their end organs. The time cou rse of the invasion of monocytes after axotomy indicates that this pro cess is not required to trigger the biochemical changes occurring in t he ganglion within the first 24 h. On the other hand, the existence of a resident population of macrophages raises the possibility that chan ges in those cells might be involved. (C) 1995 John Wiley & Sons, Inc.