Propagation of spreading depression inversely correlates with cortical myelin content

Merkler, Doron; Klinker, Florian; Jürgens, Tanja; Glaser, Raoul; Paulus, Walter; Brinkmann, Bastian G.; Sereda, Michael W.; Stadelmann, Christine; Guedes, Rubem Carlos Araújo; Brück, Wolfgang; Liebetanz, David

doi:10.1002/ana.21746

Cited by 77 publications

(52 citation statements)

References 57 publications

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“…Reduction in myelination in some areas of the brain has been documented in patients suffering from depression (Garver et al, 2008; Bartzokis, 2011; Zhang et al, 2012), and conversely, demyelinating disorders characterized by myelin loss show co-morbidity with depression (Arnett et al, 2008), but nothing has been reported about the mechanism by which demyelination progresses and so far, very little is known about the contribution of myelin plasticity as part of the hippocampal structural plasticity that occurs in depression (Merkler et al, 2009). Notably, the role of TNFR1-mediated TNF signaling in causing demyelination has been widely investigated by different authors (Arnett et al, 2001; Eugster et al, 1999; Probert et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Neuropathic pain-induced depressive-like behavior and hippocampal neurogenesis and plasticity are dependent on TNFR1 signaling

Dellarole

Morton

Brambilla

et al. 2014

Brain, Behavior, and Immunity

134

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Patients suffering from neuropathic pain have a higher incidence of mood disorders such as depression. Increased expression of tumor necrosis factor (TNF) has been reported in neuropathic pain and depressive-like conditions and most of the pro-inflammatory effects of TNF are mediated by the TNF receptor 1 (TNFR1). Here we sought to investigate: 1) the occurrence of depressive-like behavior in chronic neuropathic pain and the associated forms of hippocampal plasticity, and 2) the involvement of TNFR1-mediated TNF signaling as a possible regulator of such events. Neuropathic pain was induced by chronic constriction injury of the sciatic nerve in wild-type and TNFR1−/− mice. Anhedonia, weight loss and physical state were measured as symptoms of depression. Hippocampal neurogenesis, neuroplasticity, myelin remodeling and TNF/TNFRs expression were analyzed by immunohistochemical analysis and western blot assay. We found that neuropathic pain resulted in the development of depressive symptoms in a time dependent manner and was associated with profound hippocampal alterations such as impaired neurogenesis, reduced expression of neuroplasticity markers and myelin proteins. The onset of depressive-like behavior also coincided with increased hippocampal levels of TNF, and decreased expression of TNF receptor 2 (TNFR2), which were all fully restored after mice spontaneously recovered from pain. Notably, TNFR1−/− mice did not develop depressive-like symptoms after injury, nor were there changes in hippocampal neurogenesis and plasticity. Our data show that neuropathic pain induces a cluster of depressive-like symptoms and profound hippocampal plasticity that are dependent on TNF signaling through TNFR1.

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Section: Discussionmentioning

confidence: 99%

Neuropathic pain-induced depressive-like behavior and hippocampal neurogenesis and plasticity are dependent on TNFR1 signaling

Dellarole

Morton

Brambilla

et al. 2014

Brain, Behavior, and Immunity

134

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“…In fact, it has been demonstrated that cortical myelin content inversely correlates with CSD propagation velocity. 49 Since CSD seems to depend on neuronal activity, it is not surprising that the CSD propagation would be influenced by the inter-neuronal distance, which among other factors is influenced by the amount of myelin between the cortical cells.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of physical exercise andl-arginine on cortical spreading depression in developing rats

Monteiro

Silva

França

et al. 2011

Nutritional Neuroscience

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“…CSD propagation required high neuronal and synaptic density and was impeded by the presence of large extracellular space and an abundance of astrocytes and myelin (Bureš et al, 1974;Somjen, 2001;Merkler et al, 2009). The propagation or termination of cortical injury induced spreading depression depended on neuronal activities around peri-infarct area (Von Bornstädt et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Identification of the extent of cortical spreading depression propagation by Npas4 mRNA expression

Yoshida

Natsubori

et al. 2015

Neuroscience Research

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Propagation of spreading depression inversely correlates with cortical myelin content

Cited by 77 publications

References 57 publications

Neuropathic pain-induced depressive-like behavior and hippocampal neurogenesis and plasticity are dependent on TNFR1 signaling

Neuropathic pain-induced depressive-like behavior and hippocampal neurogenesis and plasticity are dependent on TNFR1 signaling

Differential effects of physical exercise andl-arginine on cortical spreading depression in developing rats

Identification of the extent of cortical spreading depression propagation by Npas4 mRNA expression

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