Lamotrigine effectively blocks synaptic transmission between nociceptive primary afferents and secondary sensory neurons in the rat superficial spinal dorsal horn

Zsófia Antal, Péter Szucs, M. Antal

Research output: Contribution to journalArticle

Abstract

It has been demonstrated that in the superficial spinal dorsal horn, Lamotrigine, which is known to block voltage-sensitive Na + and Ntype Ca 2+ channels, depresses neural activities evoked by sustained activation of nociceptive primary afferent fibres. In the present experiments, we study how Lamotrigine exerts its inhibitory effect on spinal nociceptive information-processing mechanisms. We show that Lamotrigine in an in vitro slice preparation effectively blocks synaptic transmission between primary afferents and secondary sensory neurons. Together with the robust increase in the failure rate and reduction in the amplitude of excitatory post-synaptic potentials (EPSPs) evoked by stimulation of nociceptive primary afferents, Lamotrigine causes a marked decrease in the number and amplitude of spontaneous EPSPs and a gradual shift of the resting membrane potential towards hyperpolarization. In addition, Lamotrigine treatment also changes the intrinsic firing pattern of superficial dorsal horn neurons. The results suggest that the effect of Lamotrigine on spinal nociceptive information-processing mechanisms is multiple: it depresses synaptic inputs from nociceptive primary afferents to secondary spinal sensory neurons and also weakens the intrinsic activities of nociceptive spinal neural circuits in the superficial spinal dorsal horn.

Original languageEnglish
Pages (from-to)22-26
Number of pages5
JournalInterventional Medicine and Applied Science
Volume3
Issue number1
DOIs
Publication statusPublished - Mar 1 2011

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Sensory Receptor Cells
Synaptic Transmission
Synaptic Potentials
Automatic Data Processing
Posterior Horn Cells
Membrane Potentials
lamotrigine
Spinal Cord Dorsal Horn

Keywords

  • dorsal horn
  • in vitro electrophysiology
  • Lamotrigine
  • nociceptive primary afferents
  • spinal cord
  • synaptic transmission

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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abstract = "It has been demonstrated that in the superficial spinal dorsal horn, Lamotrigine, which is known to block voltage-sensitive Na + and Ntype Ca 2+ channels, depresses neural activities evoked by sustained activation of nociceptive primary afferent fibres. In the present experiments, we study how Lamotrigine exerts its inhibitory effect on spinal nociceptive information-processing mechanisms. We show that Lamotrigine in an in vitro slice preparation effectively blocks synaptic transmission between primary afferents and secondary sensory neurons. Together with the robust increase in the failure rate and reduction in the amplitude of excitatory post-synaptic potentials (EPSPs) evoked by stimulation of nociceptive primary afferents, Lamotrigine causes a marked decrease in the number and amplitude of spontaneous EPSPs and a gradual shift of the resting membrane potential towards hyperpolarization. In addition, Lamotrigine treatment also changes the intrinsic firing pattern of superficial dorsal horn neurons. The results suggest that the effect of Lamotrigine on spinal nociceptive information-processing mechanisms is multiple: it depresses synaptic inputs from nociceptive primary afferents to secondary spinal sensory neurons and also weakens the intrinsic activities of nociceptive spinal neural circuits in the superficial spinal dorsal horn.",
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