Publication details

Invasion of macrophages in trigeminal ganglion compartments not related to injured nerve

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Authors

STREJČKOVÁ Lucie KLUSÁKOVÁ Ilona DUBOVÝ Petr

Year of publication 2012
Type Conference abstract
MU Faculty or unit

Central European Institute of Technology

Citation
Description In context of peripheral nerve injury macrophages play a central role in Wallerian degeneration and produce many cytokines, which contribute to development and maintenance of neuropathic pain. The goal of our work was to investigate invasion of activated macrophages not only into the trigeminal ganglia (TG) compartments containing injured but also uninjured neurons in the model of neuropathic pain. For this purpose, unilateral chronic constriction injury of the infraorbital nerve (ION) was performed. The rats were anesthetized and the left ION was exposed and tightly ligated with 6-0 silk suture. Fluorogold (FG) was injected distal to ligated nerve to visualize neurons associated with ION. The ION- and sham-operated rats were left to survive for 3 and 7 days. The naive (n=4), ION- (n=4) and sham-operated (n=4) rats were perfused with Zamboni solution and TG were dissected, fixed overnight, and washed in 20% sucrose. Longitudinal cryostat sections were incubated with rabbit polyclonal anti-ATF3 antibody to identify injured neurons and/or simultaneously incubated with mouse monoclonal antibody for ED-1. The corresponding secondary antibodies were conjugated with FITC and TRITC. The quantification of ED-1 positive cells was performed by image analysis system Lucia. Neuronal retrograde tracer (FG) visualized all TG neurons whose afferent axons contribute to ION, but ATF3 detected only injured neurons in maxillary compartment of ipsilateral TG. An increased invasion of activated ED-1+ macrophages was observed bilaterally in the TG after unilateral chronic constriction injury of the ION when compared with naive ones. The number of ED-1+ macrophages was lower in contralateral than ipsilateral TG. The TG of sham-operated rats displayed also a mild bilateral invasion of ED-1+ cells. Although injured neurons of ION lie in the maxillary compartment, a moderate invasion of macrophages was detected also in the mandibular region of TG. Our results revealed that unilateral IONL induced invasion of activated macrophages not only into compartment containing injured (ATF3+), but also uninjured neurons of TG.
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