The superoxide anion is involved in the induction of long-term potentiation in the rat somatosensory cortex in vitro

Abstract

The involvement of the superoxide anion (O 2 −) in the induction of neocortical long-term potentiation (LTP) was examined in rat brain slices containing the primary somatosensory cortex. Field potentials evoked by stimulation in cortical layer IV were recorded from layer II/III. In control experiments, tetanic high-frequency stimulation (HFS) resulted in essentially input-specific, NMDA receptor-dependent LTP (20.2±3.0% increase in field potential amplitude). When the availability of intracellular O 2 − was reduced by application of the cell membrane-permeable O 2 − scavengers MnTBAP or CP-H (spin trap), HFS-induced LTP was attenuated to 12.0±1.7% and 8.7±3.1% increase, respectively. In contrast, HFS-induced LTP was not significantly affected by the cell membrane-impermeable O 2 − scavenger superoxide dismutase (SOD). Induction of the generation of O 2 − by the cell membrane-permeable redox-cycling quinone DMNQ resulted in a HFS-independent slow-onset LTP (21.8±6.0%) in three of eight brain slices. Together, these results suggest the contribution of O 2 − to the induction of LTP in the primary somatosensory cortex by an action on intracellular induction mechanisms.