Injured primary sensory neurons switch phenotype for brain-derived neurotrophic factor in the rat

Electrical stimulation promotes peripheral axon regeneration by enhanced neuronal neurotrophin signaling

“…In contrast to highly immunoreactive motoneurons (Buck et al, 2000;Copray and Kernell, 2000), only about half of the YFP+ DRG neurons in intact mice are immunoreactive for the full length trkB molecule (English et al, 2005a). As others have shown (Michael et al, 1999;Zhou et al, 1999;Karchewski et al, 2002), axotomy results in a change in BDNF expression in DRG neurons from mainly small, presumably trkA containing cells to medium to large size neurons. In addition, the English et al Page 12 proportion of DRG neurons containing both BDNF and trkB is increased (Karchewski et al, 2002).…”

“…7F). If the sciatic nerve is transected and surgically repaired, the pattern of immunoreactivity found in the ganglia changes (Michael et al, 1999;Zhou et al, 1999;Karchewski et al, 2002). Immunoreactivity to BDNF decreases in small diameter neurons and large cells become much more strongly immunoreactive, both seven and 14 days later (Fig.…”

p38 Mitogen-Activated Protein Kinase Is Activated after a Spinal Nerve Ligation in Spinal Cord Microglia and Dorsal Root Ganglion Neurons and Contributes to the Generation of Neuropathic Pain

“…Rather, p38 is likely to be activated by nerve inflammation or degeneration. p38 activation in DRG neurons may contribute to the increased expression of many proteins, such as BDNF, ␣2␦ calcium channel, and activating transcription factor 3, that occur in injured DRG neurons (Zhou et al, 1999;Tsujino et al, 2000;Luo et al, 2001). Microarray studies have revealed that peripheral axonal injury produces changes in the expression of several hundred genes, and some of these may be regulated by p38 (Costigan et al, 2002;Xiao et al, 2002).…”

An Approach to Identify Nerve Injury-Evoked Changes that Contribute to the Development or Protect Against the Development of Sustained Neuropathic Pain

“…For example, following sciatic nerve injury there is an increase in the BDNF expression in large dorsal root ganglia sensory neurons and in satellite glia cells, while its expression is decreased in small dorsal root ganglia sensory neurons (Zhou et al, 1999), moreover the magnitude of the change in BDNF expression in dorsal root ganglia neurons depends on the site of the peripheral nerve injury (proximal vs distal) (Obata et al, 2006). These studies suggested that increases in BDNF expression in the large dorsal root ganglia sensory neurons contribute to neuropathic pain following peripheral nerve injury (Obata et al, 2006;Zhou et al, 1999). However, blocking production of BDNF by dorsal root ganglia sensory neurons, showed that BDNF in dorsal root ganglia sensory neurons, while it contributed to inflammatory pain (induced by injections of either Carrageean, NGF or Formalin), it did not contribute to the development of neuropathic pain (following L5 spinal nerve ligation) (Zhao et al, 2006).…”

“…In addition to changes in cytokines/chemokines, there are many other genes/proteins that have been found to be upregulated or downregulated in the dorsal root ganglia sensory neurons following nerve injury but in many cases their contribution to chronic pain is also complex (Birder and Perl, 1999;Krekoski et al, 1996;Lee et al, 2002;Schafers et al, 2003;Seijffers et al, 2006;Xiao et al, 2002;Zhou et al, 1999). For example, following sciatic nerve injury there is an increase in the BDNF expression in large dorsal root ganglia sensory neurons and in satellite glia cells, while its expression is decreased in small dorsal root ganglia sensory neurons (Zhou et al, 1999), moreover the magnitude of the change in BDNF expression in dorsal root ganglia neurons depends on the site of the peripheral nerve injury (proximal vs distal) (Obata et al, 2006).…”