Changes in the macrophage population of the rat superior cervical ganglion after postganglionic nerve injury.
Following peripheral nerve transection, a series of biochemical changes occurs in axons and Schwann cells both at the site of the lesion and distal to it. Macrophages differentiated from monocytes that invade the area in response to transection (elicited macrophages) and, perhaps, also macrophages normally present in the tissue (resident macrophages) play important roles in these changes. In addition, nerve transection 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 occurring in the superior cervical ganglion (SCG) after axotomy, we examined the presence of macrophages before and after axonal damage. The monoclonal antibodies ED1, ED2, and OX6 were used, each of which recognizes a somewhat different population of macrophages. Ganglia from normal rats contained a population of resident cells that were ED2+ but very few that were ED1+. Within 2 days after the post-ganglionic nerves were transected, the number of ED1+ cells increased substantially, with little change in immunostaining for ED2. These data, in combination with published studies on other tissues, suggest that ED1 in the SCG is selective for elicited macrophages and ED2 for resident macrophages. OX6 immunostaining was prominent in normal ganglia but also increased significantly after axotomy, suggesting that it reflects both macrophage populations. Systemic administration of 6-hydroxydopamine, a neurotoxin that causes the destruction of sympathetic nerve endings, also produced an increase in ED1 immunostaining. Thus, the change in ED1 immunostaining in the SCG does not require surgery, with the attendant severing of local blood vessels and connective tissue, but rather only the disconnection of sympathetic neurons from their end organs. The time course of the invasion of monocytes after axotomy indicates that this process is not required to trigger the biochemical changes occurring in the ganglion within the first 24 h. On the other hand, the existence of a resident population of macrophages raises the possibility that changes in those cells might be involved.
Schreiber
R C
RC
Department of Neurosciences, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106-4975, USA.
Shadiack
A M
AM
Bennett
T A
TA
Sedwick
C E
CE
Zigmond
R E
RE
D000818:Animals; D000911:Antibodies, Monoclonal / Q000737:chemistry; D001369:Axons / Q000502:physiology; D007091:Image Processing, Computer-Assisted; D007150:Immunohistochemistry; D008264:Macrophages / Q000502:physiology*; D008297:Male; D016627:Oxidopamine; D059348:Peripheral Nerve Injuries; D051381:Rats; D017207:Rats, Sprague-Dawley; D009418:S100 Proteins / Q000378:metabolism; D012583:Schwann Cells / Q000187:drug effects / Q000378:metabolism; D017783:Superior Cervical Ganglion / Q000166:cytology*; D013563:Sympathectomy, Chemical; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D000911:Antibodies, Monoclonal; D009418:S100 Proteins; D016627:Oxidopamine; D014446:Tyrosine 3-Monooxygenase