Arctigenin reduces neuronal responses in the somatosensory cortex via the inhibition of non-NMDA glutamate receptors

S Borbély, Gergely Jocsak, Kinga Moldovan, Lucie Sedlak, Eva Preininger, Imre Boldizsar, Attila Toth, Palmi T Atlason, Elek Molnar, Ildiko Vilagi

Research output: Contribution to journalArticle (Academic Journal)peer-review

2 Citations (Scopus)
308 Downloads (Pure)

Abstract

Lignans are biologically active phenolic compounds related to lignin, produced in different plants. Arctigenin, a dibenzylbutyrolactone-type lignan, has been used as a neuroprotective agent for the treatment of encephalitis. Previous studies of cultured rat cerebral cortical neurones raised the possibility that arctigenin inhibits kainate-induced excitotoxicity. The aims of the present study were: 1) to analyse the effect of arctigenin on normal synaptic activity in ex vivo brain slices, 2) to determine its receptor binding properties and test the effect of arctigenin on AMPA/kainate receptor activation and 3) to establish its effects on neuronal activity in vivo. Arctigenin inhibited glutamatergic transmission and reduced the evoked field responses. The inhibitory effect of arctigenin on the evoked field responses proved to be substantially dose dependent. Our results indicate that arctigenin exerts its effects under physiological conditions and not only on hyper-excited neurons. Furthermore, arctigenin can cross the blood-brain barrier and in the brain it interacts with kainate sensitive ionotropic glutamate receptors. These results indicate that arctigenin is a potentially useful new pharmacological tool for the inhibition of glutamate-evoked responses in the central nervous system in vivo.
Original languageEnglish
Pages (from-to)83-90
Number of pages8
JournalNeurochemistry International
Volume97
Early online date10 Mar 2016
DOIs
Publication statusPublished - Jul 2016

Keywords

  • Arctigenin
  • Ionotropic glutamate receptors
  • Evoked field potentials
  • Rat
  • Brain slices
  • In vivo experiments

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