The analgesic effects of botulinum neurotoxin by modulating pain-related receptors; A literature review

Botulinum neurotoxins (BoNTs) are being explored for their potential to alleviate pain, particularly in neurological conditions. One proposed mechanism is their ability to disrupt the transmission of pain signals by interfering with the movement of pain-related receptors to the neuronal cell membrane. BoNTs can disrupt the integration of synaptic vesicles with the cellular membrane. This disruption affects the transport of various receptors, including TRP channels, calcium channels, sodium channels, purinergic receptors, neurokinin-1 receptors, and glutamate receptors. Furthermore, BoNTs also interact with the opioidergic and GABAergic systems, which play critical roles in pain modulation. A deeper understanding of these mechanisms could pave the way for developing innovative pain management therapies.

• 1
  BoNTs inhibit the release of neurotransmitters involved in the pain pathway, including CGRP, glutamate, substance P, and ATP, by suppressing SNARE proteins.
• 2
  BoNTs modulate the expression and translocation of various receptors, including TRP ion channels, sodium channels, calcium channels, purinergic receptors, NK-1 receptor, and glutamate receptors.
• 3
  BoNTs modulate the endogenous opioid system and GABAergic pathways, thereby reducing pain sensation.