RAPID COMMUNICATION Cell-Permeable Scavengers of Superoxide Prevent Long-Term Potentiation in Hippocampal Area CA1

Klann, Eric. Cell-permeable scavengers of superoxide prevent shown that extracellular application of superoxide dismulong-term potentiation in hippocampal area CA1. J. Neurophysiol. tase (SOD) and catalase, enzymes that catalyze the re80: 452–457, 1998. Long-term potentiation (LTP) in hippocampal moval of superoxide and hydrogen peroxide, respectively, area CA1 is generally dependent on N-methyl-D-aspartate attenuates LTP induction in area CA1 (Klann et al. 1998) . (NMDA) receptor activation. Reactive oxygen species (ROS), In agreement with these findings, transgenic mice that including superoxide, are produced in response to NMDA receptor overexpress Cu/Zn SOD have impaired LTP that can be activation in a number of brain regions, including the hipppocamrescued partially by catalase (Gahatan et al. 1998) . Fipus. In this study, two cell-permeable manganese porphyrin comnally, incubation of hippocampal slices with 5,5 dimethyl pounds that mimic superoxide dismutase (SOD) were used to depyrolline 1-oxide (DMPO) , an electron spin resonance termine whether production of superoxide is required for the induction of LTP in area CA1 of rat hippocampal slices. Incubation of spin trap reagent that is capable of removing superoxide, hippocampal slices with either Mn(III) tetrakis (4-benzoic acid) also attenuates LTP induction (Klann et al. 1998) . porphyrin (MnTBAP) or Mn(III) tetrakis (1-methyl-4-pyridyl) Extracellular application of cell-impermeable comporphyrin (MnTMPyP) prevented the induction of LTP. Incubation pounds, such as SOD, catalase, and DMPO, to slices likely of slices with either light-inactivated MnTBAP or light-inactivated results in the scavenging of superoxide extracellularly. MnTMPyP had no effect on induction of LTP. Neither MnTBAP The observation that these compounds attenuate and do nor MnTMPyP was able to reverse preestablished LTP. These not completely block LTP (Klann et al. 1998) could be observations suggest that production of superoxide occurs in rebecause of intracellular actions of superoxide that are unsponse to LTP-inducing stimulation and that superoxide is necesaffected by extracellular scavengers after LTP-inducing sary for the induction of LTP. HFS. Therefore intracellular actions of superoxide might