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

Heusler, Peter; Boehmer, Gerd

doi:10.1016/j.brainres.2004.07.047

Cited by 11 publications

(3 citation statements)

References 42 publications

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“…BVR À/À neurons are also hyper-sensitive to O 2 ,À over H 2 O 2 (Figure S4A). Ex vivo, DHE fluorescence suggests that BVR Lafon-Cazal et al, 1993), which functions as a second messenger in long-term potentiation and other redox signaling axes (Gao et al, 2007;Heusler and Boehmer, 2004;Klann, 1998;Wang et al, 1996). BVR À/À mice exhibit Gauged by real-time DHE fluorescence, we observe that treating neurons with NMDA stimulates O 2 ,À signaling, consistent with previous reports (Figure 4D) (Bindokas et al, 1996;Brennan et al, 2009;Lafon-Cazal et al, 1993).…”

Section: Nmda Receptors Signal Via Osupporting

confidence: 91%

Bilirubin Links Heme Metabolism to Neuroprotection by Scavenging Superoxide

Vasavda

Kothari

Malla

et al. 2019

Cell Chemical Biology

107

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Section: Nmda Receptors Signal Via Osupporting

confidence: 91%

Bilirubin Links Heme Metabolism to Neuroprotection by Scavenging Superoxide

Vasavda

Kothari

Malla

et al. 2019

Cell Chemical Biology

107

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“…In addition, long-term potentiation (LTP), a form of func-tional neuroplasticity, was also found to be associated with pain processing in recent years, except for its wide use as a unique synaptic model for learning and memory [48][49][50]. Actually, there have been a number of previous studies investigating LTP phenomenon in multiple painrelated CNS regions, including the spinal cord dorsal horn [51][52][53], primary somatosensory cortex (S1 area) [54,55], amygdala [55,56], anterior cingulate cortex [55,[57][58][59][60][61] and so on. As regards the HF, an enhanced LTP by pain was also reported in one previous study [62].…”

Section: Introductionmentioning

confidence: 99%

Nociception-Induced Spatial and Temporal Plasticity of Synaptic Connection and Function in the Hippocampal Formation of Rats: a Multi-Electrode Array Recording

et al. 2009

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BackgroundPain is known to be processed by a complex neural network (neuromatrix) in the brain. It is hypothesized that under pathological state, persistent or chronic pain can affect various higher brain functions through ascending pathways, leading to co-morbidities or mental disability of pain. However, so far the influences of pathological pain on the higher brain functions are less clear and this may hinder the advances in pain therapy. In the current study, we studied spatiotemporal plasticity of synaptic connection and function in the hippocampal formation (HF) in response to persistent nociception.ResultsOn the hippocampal slices of rats which had suffered from persistent nociception for 2 h by receiving subcutaneous bee venom (BV) or formalin injection into one hand paw, multisite recordings were performed by an 8 × 8 multi-electrode array probe. The waveform of the field excitatory postsynaptic potential (fEPSP), induced by perforant path electrical stimulation and pharmacologically identified as being activity-dependent and mediated by ionotropic glutamate receptors, was consistently positive-going in the dentate gyrus (DG), while that in the CA1 was negative-going in shape in naïve and saline control groups. For the spatial characteristics of synaptic plasticity, BV- or formalin-induced persistent pain significantly increased the number of detectable fEPSP in both DG and CA1 area, implicating enlargement of the synaptic connection size by the injury or acute inflammation. Moreover, the input-output function of synaptic efficacy was shown to be distinctly enhanced by the injury with the stimulus-response curve being moved leftward compared to the control. For the temporal plasticity, long-term potentiation produced by theta burst stimulation (TBS) conditioning was also remarkably enhanced by pain. Moreover, it is strikingly noted that the shape of fEPSP waveform was drastically deformed or split by a TBS conditioning under the condition of persistent nociception, while that in naïve or saline control state was not affected. All these changes in synaptic connection and function, confirmed by the 2-dimentional current source density imaging, were found to be highly correlated with peripheral persistent nociception since pre-blockade of nociceptive impulses could eliminate all of them. Finally, the initial pharmacological investigation showed that AMPA/KA glutamate receptors might play more important roles in mediation of pain-associated spatiotemporal plasticity than NMDA receptors.ConclusionPeripheral persistent nociception produces great impact upon the higher brain structures that lead to not only temporal plasticity, but also spatial plasticity of synaptic connection and function in the HF. The spatial plasticity of synaptic activities is more complex than the temporal plasticity, comprising of enlargement of synaptic connection size at network level, deformed fEPSP at local circuit level and, increased synaptic efficacy at cellular level. In addition, the multi-synaptic model established in the pres...

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“…However, several observations suggest that both O

_{2}^{−·}

· and H 2 O 2 also play a positive facilitatory role in LTP forms of synaptic plasticity in the mammalian hippocampus. For example, removal of O

_{2}^{−·}

· by CuZnSOD (SOD1) enzyme preparations, by cell‐permeable scavengers, or by overexpression of either SOD1 or extracellular SOD (EC‐SOD) in adult transgenic mice has been shown to inhibit certain forms of LTP induced by high frequency stimulation (HFS; Klann,1998; Klann et al,1998; Gahtan et al,1998; Thiels et al,2000; Kamsler and Segal,2003b; Wang et al,2004; Heusler and Boehmer,2004). A recent study suggest that O

_{2}^{−·}

· is normally generated at synapses by membrane‐bound NADPH oxidase, which also is required for N‐methyl‐D‐aspartate (NMDA) receptor‐dependent activation of extracellular signal‐regulated kinase (ERK) in hippocampal area CA1 (Tejada‐Simon et al,2005; Kishida et al,2005).…”

mentioning

confidence: 99%

Age‐dependent modulation of hippocampal long‐term potentiation by antioxidant enzymes

Watson

Arnold

et al. 2006

J of Neuroscience Research

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Oxidative stress has long been associated with normal aging and age-related neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD). However, it is now evident that reactive oxygen species (ROS) such as superoxide (O(2-*)) and hydrogen peroxide (H(2)O(2)) also play pivotal roles in normal cell signaling. The focus of the present study was to examine the effects of the antioxidant enzymes CuZnSOD (SOD1) and catalase, which produce and remove H(2)O(2), respectively, on long-term potentiation (LTP) forms of synaptic plasticity during aging. Consistent wth previous studies, LTP, when induced in vitro in CA1 of the hippocampus with a high-frequency stimulation protocol, is significantly reduced in slices from older mice (22-26 months) relative to younger mice (2-4 months). Neither knockout of the endogenous catalase gene (Cat KO) nor acute enzymatic treatment with SOD1 altered LTP in slices from adult mice. Conversely, enzymatic applications of SOD1 inhibited LTP in slices from older mice. A much different set of results emerges with exogenous applications of catalase to hippocampal slices. Catalase significantly inhibited LTP in slices from adult mice but reversed age-related LTP deficits in slices from older mice. Measurements of H(2)O(2) showed that exogenous treatments with catalase lowered H(2)O(2) in synapse-enriched synaptoneurosome (SN) fractions prepared from adult mice. Notably, SNs from both Cat KO and old mice were deficient in removing extracellular challenges of H(2)O(2). Overall, the results suggest that dynamic alterations in extracellular H(2)O(2) metabolism affect synaptic plasticity in the hippocampus during aging.

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

Cited by 11 publications

References 42 publications

Bilirubin Links Heme Metabolism to Neuroprotection by Scavenging Superoxide

Bilirubin Links Heme Metabolism to Neuroprotection by Scavenging Superoxide

Nociception-Induced Spatial and Temporal Plasticity of Synaptic Connection and Function in the Hippocampal Formation of Rats: a Multi-Electrode Array Recording

Age‐dependent modulation of hippocampal long‐term potentiation by antioxidant enzymes

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