Mechanism of dorsal root ganglion stimulation for pain relief in painful diabetic polyneuropathy is not dependent on GABA release in the dorsal horn of the spinal cord.
Animals
Diabetic Neuropathies
/ complications
Electric Stimulation Therapy
/ methods
Electrodes, Implanted
Female
Ganglia, Spinal
/ physiology
Hyperalgesia
Pain
/ etiology
Pain Management
/ methods
Pain Measurement
Rats
Rats, Sprague-Dawley
Spinal Cord Dorsal Horn
/ metabolism
gamma-Aminobutyric Acid
/ metabolism
animal model
dorsal horn
dorsal root ganglion stimulation
painful diabetic polyneuropathy
rats
spinal cord
γ-aminobutyric acid
Journal
CNS neuroscience & therapeutics
ISSN: 1755-5949
Titre abrégé: CNS Neurosci Ther
Pays: England
ID NLM: 101473265
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
received:
25
02
2019
revised:
17
06
2019
accepted:
24
06
2019
pubmed:
25
7
2019
medline:
29
6
2021
entrez:
24
7
2019
Statut:
ppublish
Résumé
It is hypothesized that dorsal root ganglion stimulation (DRGS), sharing some of the mechanisms of traditional spinal cord stimulation (SCS) of the dorsal columns, induces γ-aminobutyric acid (GABA) release from interneurons in the spinal dorsal horn. We used quantitative immunohistochemical analysis in order to investigate the effect of DRGS on intensity of intracellular GABA-staining levels in the L4-L6 spinal dorsal horn of painful diabetic polyneuropathy (PDPN) animals. To establish the maximal pain relieving effect, we tested for mechanical hypersensitivity to von Frey filaments and animals received 30 minutes of DRGS at day 3 after implantation of the electrode. One day later, 4 Sham-DRGS animals and four responders-to-DRGS received again 30 minutes of DRGS and were perfused at the peak of DRGS-induced pain relief. No significant difference in GABA-immunoreactivity was observed between DRGS and Sham-DRGS in lamina 1-3 of the spinal levels L4-6 neither ipsilaterally nor contralaterally. Dorsal root ganglion stimulation does not induce GABA release from the spinal dorsal horn cells, suggesting that the mechanisms underlying DRGS in pain relief are different from those of conventional SCS. The modulation of a GABA-mediated "Gate Control" in the DRG itself, functioning as a prime Gate of nociception, is suggested and discussed.
Identifiants
pubmed: 31334605
doi: 10.1111/cns.13192
pmc: PMC6930820
doi:
Substances chimiques
gamma-Aminobutyric Acid
56-12-2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
136-143Informations de copyright
© 2019 The Authors. CNS Neuroscience & Therapeutics Published by John Wiley & Sons Ltd.
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