Changes of molecular composition in the basal laminae around the neuron-satellite cell units of the dorsal root ganglia following constriction nerve injury are related with invasion of ED-1 positive macrophages
Authors | |
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Year of publication | 2005 |
Type | Article in Proceedings |
Conference | VII.European Meeting on Glial Cell Function in Health and Disease |
MU Faculty or unit | |
Citation | |
Field | Neurology, neurosurgery, neurosciences |
Keywords | neuropathic; pain |
Description | A constriction injury (CI) of the peripheral nerve may stimulate invasion of the sympathetic fiber sprouts into the dorsal root ganglia (DRG) to form sympathetic baskets around DRG neurons. Changes of extracellular matrix composition including the basal lamina may result in a condition of DRG stimulating the growth of sympathetic sprouts. The experimental CI was applied ipsilaterally on the spinal nerve at a 4mm distance from DRG as well as on the sciatic nerve at a 40 mm distance from DRG of Wistar rats. Both ipsilateral and contralateral DRG (L4-L5) were removed 1, 2 and 4 weeks after the operation. The DRG (L4-L5) of intact (naive) rats were used as a control. Cryostat sections were simultaneously immunostained for laminin-1, dystroglycan, nidogen, collagen-IV, concanavalin-A, (con-A) and ED-1. Immunofluorescence staining (IF) for laminin-1 around ipsilateral neuron-satellite cell units was a mosaic following CI in contrast to naive and contralateral DRG. The mosaic laminin distribution was confirmed by con-A. Simultaneous staining for nidogen and collagen-IV confirmed changes of molecular composition in the basal laminae around the neuron-satellite cell units after CI. The molecular changes of the basal laminae correlated with invasion of ED-1 positive macrophages and their close relationships with the DRG neuron-satellite cell units. The results suggested that ED-1+ macrophages play a crucial role for the growth of sympathetic sprouts close to the DRG neurons and for development of sympathetically maintained pain. Supported by 309/03/1199 and MSM0021622404. |
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