The effects of the superoxide dismutase mimetic, MnTMPyP, post hypoxia and oxygen glucose deprivation in isolated rat hippocampal slices

An Electrophysiological and Proteomic Analysis of the Effects of the Superoxide Dismutase Mimetic, MnTMPyP, on Synaptic Signalling Post-Ischemia in Isolated Rat Hippocampal Slices

“…In these electrophysiological experiments, a shorter episode of OGD was used in order to be able to obtain a recovery of fEPSP and induce LTP. Application of MnTMPyP (25 µM) prior to a 10 min OGD induced a similar lack of fEPSP recovery to the 15 min OGD previously reported [ 20 ], an effect that was not seen with 2.5 µM. Proteomic analysis of 20 min OGD without MnTMPyP shows upregulation of synaptic plasticity and LTP.…”

“…It has previously been reported that application of MnTMPyP (25 µM) modulates synaptic transmission recovery after an insult of 20 min OGD in the CA1 area of the hippocampus [ 20 ]. In order to evaluate the effect of the superoxide scavenger on post-ischemic synaptic plasticity, a 10 min model of oxygen–glucose deprivation was used.…”

“…Despite the vast research carried out on the neuroprotective role of antioxidants in counteracting oxidative stress, there is still a gap in the literature on how exactly they modulate synaptic transmission and plasticity [ 6 ]. The modulatory effects of antioxidant treatment with MnTMPyP on synaptic transmission and neuronal viability post-ischemia have been previously investigated [ 20 ]. In these studies, a high concentration of MnTMPyP (25 µM) induced a decreased fEPSP recovery post-ischemia in the CA1 region of the hippocampus.…”

“…Shahraki and Stone (2004) reported that superoxides can prevent the protective effect of adenosine presynapically and that this antagonism of adenosine responses may contribute to the injurious effects of ROS [ 57 ]. In addition, the application of DPCPX, DCKA and AP5 have been previously reported to reverse the protective effects of MnTMPyP on synaptic transmission post-ischemia [ 20 ]. It has been reported that superoxide is produced by NMDA receptors in an attempt to achieve a state of NMDA receptor hypofunction in order to limit damaging Ca 2+ influx [ 58 ].…”

“…In an in vivo study in mice exposed to brief and repetitive episodes of I-RI, the administration of MnTMPyP rescued synaptic plasticity, ameliorating the deleterious effect of the hypoxic insult on synaptogenesis [ 18 , 19 ]. We have previously shown that the superoxide dismutase mimetic MnTMPyP has a neuroprotective effect in hippocampal slices exposed to hypoxia and oxygen–glucose deprivation (OGD) [ 20 ].…”