Effects of Peripheral Inflammation on Brain-Derived Neurotrophic Factor and TrkB in Rat Dorsal Root Ganglia and Spinal Cord / 대한해부학회지

ABSTRACT

Recent study showed that peripheral inflammation induced an increased expression of brain-derived neurotrophic factor (BDNF) mRNA which was mediated by nerve growth factor in the dorsal root ganglion (DRG). Therefore, it is conceivable that peripheral inflammation may induce an increase in BDNF synthesis in DRG and consequently enhance the level of BDNF in the spinal cord and that gene expression of trkB mRNA may be altered. In the present study, we evaluated changes in BDNF-immunoreactivity and trkB mRNA in the DRG and spinal cord by means of immunohis-tochemistry and RT-PCR, respectively, following peripheral tissue inflammation produced by intraplantar injection of Freund's adjuvant into rat paws. In addition, coexistence of BDNF and preprotachykinin (PTT) mRNAs, BDNF and CGRP mRNAs or BDNF and trkB mRNAs in the DRG following inflammation was observed by means of in situ hybridization. The results obtained were as follows; 1. Inflammation induced a significant increase of the number of BDNF-immunoreactive (IR) neurons in the ipsilateral DRGs. The increase was observed 1 and 3 days after injection of adjuvant, and the levels had returned to normal by 7 days. In the spinal cord, inflammation also induced an elevation in the expression of BDNF-IR terminals in the medial superficial layers of the ipsilateral dorsal horn and in lamina V 1 and 3 days after injection. 2. There was significant increase of truncated trkB (t-trkB) mRNA in the ipsilateral DRG 3 days following inflammation. Changes in the expression of trkB mRNA in the DRG or trkB and t-trkB mRNAs in the spinal cord were not observed. 3. Many neurons showed increased coexistence of BDNF and PTT mRNAs or BDNF and CGRP mRNAs in the DRG following inflammation. 4. Few neurons showed coexistence of BDNF and trkB mRNAs in the DRG following inflammation. The results suggest a paracrine function for BDNF within the DRG in addition to an important role related with nociception following peripheral inflammation.