Abstract
Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic factor family of signaling molecules. Since its discovery over three decades ago, BDNF has been identified as an important regulator of neuronal development, synaptic transmission, and cellular and synaptic plasticity and has been shown to function in the formation and maintenance of certain forms of memory. Neural plasticity that underlies learning and memory in the hippocampus shares distinct characteristics with spinal cord nociceptive plasticity. Research examining the role BDNF plays in spinal nociception and pain overwhelmingly suggests that BDNF promotes pronociceptive effects. BDNF induces synaptic facilitation and engages central sensitization-like mechanisms. Also, peripheral injury-induced neuropathic pain is often accompanied with increased spinal expression of BDNF. Research has extended to examine how spinal cord injury (SCI) influences BDNF plasticity and the effects BDNF has on sensory and motor functions after SCI. Functional recovery and adaptive plasticity after SCI are typically associated with upregulation of BDNF. Although neuropathic pain is a common consequence of SCI, the relation between BDNF and pain after SCI remains elusive. This article reviews recent literature and discusses the diverse actions of BDNF. We also highlight similarities and differences in BDNF-induced nociceptive plasticity in naïve and SCI conditions.
Highlights
After three decades of research, significant advances have been made in unraveling the cellular effects of brain-derived neurotrophic factor (BDNF)
Our studies focused on unraveling these differential effects BDNF has on spinal networks in uninjured and injured spinal cord
Deductions made from several studies including some from our laboratories overwhelming show that as it relates to nociceptive processes, whereas BDNF exerts pronociceptive actions in the absence of injury, no such effect is observed after injury, at least acutely
Summary
After three decades of research, significant advances have been made in unraveling the cellular effects of brain-derived neurotrophic factor (BDNF). (i) The TrkB receptor dimerizes, which leads to (ii) autophosphorylation of the receptor and (iii) the subsequent activation of intracellular signaling cascades These include the mitogen-activated protein kinase (MAPK), phospholipase C-γ (PLC-γ), and phosphatidylinositol-3 kinase (PI3K) cascades (see [3,4,5,6,7] and Figure 1). While BDNF does not necessarily initiate an event such as a synaptic, sensory, or motor response, it can modify the response, exerting inhibition or facilitation Such effects have been observed in the dorsal root ganglia, spinal cord, and various brain regions, where BDNF actions are typically associated with increased excitability, pronociception, learning, and memory. We will (1) offer an overview of BDNF as a modulator of neural plasticity and (2) discuss the differential roles BDNF plays in spinal plasticity in intact and injured spinal cord, focusing on BDNF’s effect on nociceptive plasticity. Despite the significant progress that has been made over the last 30 years, we will show that many questions remain unanswered
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