Bilal F Shanti*, Zaynab I Shanti and Ihsan F Shanti

Department of Pain Medicine, Omnia Pain Consultants, USA

*Corresponding Author: Bilal F Shanti, Department of Pain Medicine, Omnia Pain Consultants, USA.

Received: September 10, 2022; Published: November 08, 2022

Abstract

This manuscript will review the crucial role of BDNF as a pain mediator and modulator of neuroinflammation and neuropathic pain. BDNF belongs to of the neurotrophin family of growth factors that is encoded by the bdnf gene. Its role as modulator was found to act on neuronal excitability and synaptic plasticity has triggered huge interest in neurobiological pain research. This pointed to renewed interest as a potential target for pharmacological agents in its long cascade of mechanism of actions.

There is no clear-cut explanation on how BDNF works. One thing we know is that BDNF mechanism of action depends on whether we are dealing with a normal nerve, after an acute injury, or following chronic state. It is considered a major tertiary mediator in the genesis of central sensitization. It mediates inflammatory and peripheral injury-induced pain and play a role by increasing dorsal horn excitability. Hence disrupting these cycles can potentially curb the genesis of chronic pain.

Some suggested mechanisms of action of BDNF in neuropathic pain is via enhanced neuronal sensitivity to painful stimuli and an enhanced co-expression of thermo-TRP channels. Another possible mechanism entails the involvement of microglia in pain. Following a peripheral injury, GABA-BDNF plays an essential role in formation of neuropathic pain. BDNF increases both the excitatory and inhibitory synaptic drives to putative excitatory interneurons while attenuating synaptic transmission to inhibitory GABAergic neurons.

In the absence of any injury and in normal states, BDNF-mediated effects contribute to pain. An increase in BDNF and TrkB expression activate MAPK/ERK and PLC-PKC kinase pathways.

In the acute stage of nerve injury, the levels of both BDNF and TrkB are decreased in the spinal cord dorsal horn. During the chronic stage of injury, pERK levels are also noted to increase. This may result from increases in both BDNF-TrkB signaling and TNF𝛼-TNFR signaling.

BDNF may also potentially modulate spinal neuron responsiveness by potentiation of postsynaptic N-methyl-D-aspartate (NMDA) receptors.

BDNF noticeably enhanced the frequency of miniature excitatory postsynaptic currents (EPSCs) recorded in superficial dorsal horn neurons.

All these mechanisms and theories may potentially be a dream for clinicians to work on and modulate pain.

Keywords:BDNF; TrkB; Plasticity; Neuropathic Pain; Neurotrophins; Neuroinflammation; Plasticity; NMDA Receptors; IL-1β; GABA; Central Sensitization

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Citation

Citation: Bilal F Shanti., et al. “BDNF: The Old-New Pain Mediator and Modulator of Neuropathic Pain and Neuroinflammation". Acta Scientific Neurology 5.12 (2022): 33-42.

Copyright

Copyright: © 2022 Bilal F Shanti., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.