Ipsilateral L5 Dorsal Root Ganglion Research Articles

Expression of mRNA for neurotrophic factors and their receptors in the rat dorsal root ganglion and sciatic nerve following nerve injury.

The adult rat dorsal root ganglion (DRG) produces mRNA for the neurotrophic factors nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) and contains large populations of neurons responsive to these factors. We report that following a focal crush injury of the sciatic nerve, NGF mRNA expression increases threefold and BDNF mRNA two-fold, in the ipsilateral L4 and L5 DRGs. The mRNAs encoding the cognate neurotrophin receptors, p75NGFR, trkA, and trkB were expressed in the DRG throughout the post-injury time course, suggesting that DRG neurons remain responsive to both NGF and BDNF. p75NGFR mRNA levels became transiently depressed in the DRG during the first several days after the lesion but returned to normal within 1 week. trkB mRNA was expressed in the normal sciatic nerve and levels were not altered by nerve crush. RNase protection assays detected both full-length and truncated trkB transcripts in the DRG, but only truncated trkB mRNA, lacking the tyrosine kinase domain, was detected in the sciatic nerve. Likewise, trkA transcripts were not detected by RNase protection in normal sciatic nerve or in a segment of nerve distal to the crush site. These results are consistent with a model in which regenerating sensory neurons are supported by neurotrophic factors synthesized within the DRG.

Nitric oxide synthase-like immunoreactivity in lumbar dorsal root ganglia and spinal cord of rat and monkey and effect of peripheral axotomy.

With the immunofluorescence technique, nitric oxide synthase (NOS)-like immunoreactivity (LI) was found in a few medium-sized and small sensory neurons in lumbar (L) 4 and L5 dorsal root ganglia (DRG) of normal rat, and in most of these neurons, NOS-LI coexisted with calcitonin gene-related peptide and sometimes with substance P and galanin. NOS-immunoreactive nerve fibers, terminals and small neurons were also located in the dorsal horn of the segments 4 and 5 of the rat lumbar spinal cord with the highest density in inner lamina II. Many NOS-positive neurons and fibers were seen in the area around the central canal. A sparse network of NOS-immunoreactive nerve fibers was found in the ventral horn. After unilateral sciatic nerve cut in the rat, the number of NOS-positive neurons increased in the ipsilateral L4 and L5 DRGs, mainly in medium and small neurons, but also in some large neurons and very small neurons. NOS-LI could now also be seen in the ipsilateral dorsal roots, and in an increased number of fibers and terminals in both outer and inner lamina II of the ipsilateral dorsal horn. The number of NOS-immunoreactive neurons in lamina II of the ipsilateral dorsal horn was reduced. In the monkey L4 and L5 DRGs, many small neurons were NOS-immunoreactive, but only a few weakly stained nerve fibers and terminals were found in laminae I-IV of the dorsal horn at L4 and L5 lumbar levels. A few NOS-positive neurons were present in lamina X. The number of NOS-immunoreactive neurons was somewhat reduced in DRGs 14 days after peripheral axotomy, but no certain effect was seen in the dorsal horn. These results, together with earlier in situ hybridization studies, demonstrate that axotomy in rat induces a marked upregulation of NOS synthesis in primary sensory neurons, thus suggesting a role for NO in lesioned sensory neurons. In contrast, no such effect was recorded in monkey, perhaps indicating distinct species differences.

Movement of horseradish peroxidase after its entry into intact and damaged peripheral nerve axons

After application of a solution of horseradish peroxidase (HRP) around intact sciatic nerve axons in the rat, numerous HRP-labeled neurons were found in the ipsilateral L5 dorsal root ganglion and spinal cord ventral horn. These findings indicate that HRP enters intact peripheral nerve axons, and is transported retrogradely from its site of entry to their cell bodies of origin.