A role for sodium and chloride in kainic acid-induced beading of inhibitory interneuron dendrites

Al-Noori, Salwa; Swann, John W.

doi:10.1016/s0306-4522(00)00384-5

Cited by 53 publications

(38 citation statements)

References 42 publications

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“…17 Studies have shown that excessive Na ϩ influx through glutamate receptor channels is both necessary and sufficient to induce dendritic beading in excitotoxic conditions, whereas Ca 2ϩ influx is unnecessary. 36 Our data also showed that MAP2 signals were decreased in both the chronic EAE (B). Analysis of variance tests showed significant differences (P Ͻ 0.01) in all four groups of data, and post hoc tests were applied to examine the significance of differences between individual subgroups.…”

Section: Discussionsupporting

confidence: 70%

Dendritic and Synaptic Pathology in Experimental Autoimmune Encephalomyelitis

Zhu

Luo

Moore

et al. 2003

The American Journal of Pathology

110

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Evidence has shown that excitotoxicity may contribute to the loss of central nervous system axons and oligodendrocytes in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). Because dendrites and synapses are vulnerable to excitotoxicity, we examined these structures in acute and chronic models of EAE. Immunostaining for microtubule-associated protein-2 showed that extensive dendritic beading occurred in the white matter of the lumbosacral spinal cord (LSSC) during acute EAE episodes and EAE relapses. Retrograde labeling confirmed that most motoneuron dendrites were beaded in the white matter of the LSSC in acute EAE. In contrast, only mild swelling was observed in the gray matter of the LSSC. Dendritic beading showed marked recovery during EAE remission and after EAE recovery. In addition, synaptophysin, synapsin I, and PSD-95 immunoreactivities were significantly reduced in both the gray and white matter of the LSSC during acute EAE episodes and EAE relapses, but showed partial recovery during EAE remission and after EAE recovery. Pathologically, both dendritic beading and the reduction in synaptic protein immunoreactivity were well correlated with inflammatory cell infiltration in the LSSC at different EAE stages. We propose that dendritic and synaptic damage in the spinal cord may contribute to the neurological deficits in EAE. Central nervous system (CNS) inflammation and neurodegeneration are two major pathological processes in multiple sclerosis (MS). Understanding the pathology and mechanisms of CNS degeneration in MS is essential for protecting neural structures and functions in MS patients. In addition to the demyelination and the loss of oligodendrocytes, axonal degeneration in MS has received substantial attention. It has been realized that axonal loss starts early in the disease course, 1,2 and that the accumulation of axonal damage parallels in general the progressive neurological dysfunction in MS patients.3

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Section: Discussionsupporting

confidence: 70%

Dendritic and Synaptic Pathology in Experimental Autoimmune Encephalomyelitis

Zhu

Luo

Moore

et al. 2003

The American Journal of Pathology

110

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“…In vitro exposure to sublethal excitotoxic stimuli can cause dendritic beading (10,14,15), retraction of spines (16), and loss of synaptic transmission (17) that can all recover after washout of the excitotoxin. Beaded neurites can recover in vivo following β-amyloid clearance in a murine model for Alzheimer disease (18), and dendritic beading and recovery parallel the onset and remission of reversible neurologic deficits in experimental autoimmune encephalitis (19) and a model for noise-induced hearing loss (20).…”

Section: Introductionmentioning

confidence: 99%

Synaptic activity becomes excitotoxic in neurons exposed to elevated levels of platelet-activating factor

Bellizzi¹

2005

Journal of Clinical Investigation

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Neurologic impairment in HIV-1-associated dementia (HAD) and other neuroinflammatory diseases correlates with injury to dendrites and synapses, but how such injury occurs is not known. We hypothesized that neuroinflammation makes dendrites susceptible to excitotoxic injury following synaptic activity. We report that platelet-activating factor, an inflammatory phospholipid that mediates synaptic plasticity and neurotoxicity and is dramatically elevated in the brain during HAD, promotes dendrite injury following elevated synaptic activity and can replicate HIV-1-associated dendritic pathology. In hippocampal slices exposed to a stable platelet-activating factor analogue, tetanic stimulation that normally induces long-term synaptic potentiation instead promoted development of calcium-and caspase-dependent dendritic beading. Chemical preconditioning with diazoxide, a mitochondrial ATP-sensitive potassium channel agonist, prevented dendritic beading and restored long-term potentiation. In contrast to models invoking excessive glutamate release, these results suggest that physiologic synaptic activity may trigger excitotoxic dendritic injury during chronic neuroinflammation. Furthermore, preconditioning may represent a novel therapeutic strategy for preventing excitotoxic injury while preserving physiologic plasticity.

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“…Low-Na + buffer, TTX, glutamate receptor antagonists, Na + and Ca 2+ exclusion Several different experimental conditions induce bead formation in the dendrites and axons of hippocampal, cerebellar, cortical, and spinal cord neurons (e.g., Ramón y Cajal, 1899; Bindokas and Miller, 1995;Emory and Lucas, 1995;Park et al, 1996;Kirov et al, 2004;Lavenex et al, 2009), and a number of treatments have been found to counteract this beading (Ramón y Cajal, 1899; Bindokas and Miller, 1995;Park et al, 1996;Hasbani et al, 1998;Al-Noori and Swann, 2000;Oliva et al, 2002;Kirov et al, 2004;Takeuchi et al, 2005;Zhang et al, 2007). For example, glutamate receptor agonists (e.g., kainate) and voltage-gated Na + channel agonists (e.g., veratridine) lead to marked beading, and this can be averted by exclusion of extracellular Na + and Ca 2+ ions, addition of glutamate receptor antagonists, or inclusion of voltage-gated Na + channel antagonists (e.g., tetrodotoxin, lidocaine).…”

Section: Osmolaritymentioning

confidence: 99%

“…Firstly, RGC beading clearly differs from that in hippocampal, cerebellar, cortical, and spinal cord neurons in that it is not blocked by tetrodotoxin (Hasbani et al, 1998;Ikegaya et al, 2001), glutamate receptor antagonists (Park et al, 1996;Al-Noori and Swann, 2000;Oliva et al, 2002;Takeuchi et al, 2005), or Ca 2+ omission (Bindokas and Miller, 1995), and it is not induced by low temperature (Emory and Lucas, 1995;Kirov et al, 2004;Zhang et al, 2007). This conclusion is most directly supported by our observation that beading occurs in Na + -and Ca 2+ -free fixative (viz., FA diluted in HEPES; Fig.…”

Section: Bead Formation In Other Central Neuronsmentioning

confidence: 99%

“…Based in part on studies of other neuronal preparations, we test here the possibility that bead formation is induced by FA concentration, fixative osmolarity, temperature, and Na + influx via voltage-gated Na + channels or glutamate-gated cation channels . Our results indicate that retinal ganglion cells differ from hippocampal, cerebellar, cortical, and spinal cord neurons in that beading is not precluded by glutamate receptor antagonists, tetrodotoxin, extracellular Ca 2+ ion exclusion, or temperature shifts (cf., Bindokas and Miller, 1995;Emory and Lucas, 1995;Park et al, 1996;Hasbani et al,1998;Al-Noori and Swann, 2000;Oliva et al, 2002;Kirov et al, 2004;Takeuchi et al, 2005;Zhang et al, 2007). Moreover, we describe a modification of FA-based fixatives that prevents bead formation in adult rat and rabbit retinal ganglion cells.…”

Section: Introductionmentioning

confidence: 98%

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Moniliform deformation of retinal ganglion cells by formaldehyde‐based fixatives

Stradleigh

Greenberg

Partida

et al. 2015

J of Comparative Neurology

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Protocols for characterizing cellular phenotypes commonly use chemical fixatives to preserve anatomical features, mechanically stabilize tissue, and stop physiological responses. Formaldehyde, diluted in either phosphate-buffered saline or phosphate buffer, has been widely used in studies of neurons, especially in conjunction with dyes and antibodies. However, previous studies have reported that these fixatives induce the formation of bead-like varicosities in the dendrites and axons of brain and spinal cord neurons. We report here that these formaldehyde formulations can induce bead formation in the dendrites and axons of adult rat and rabbit retinal ganglion cells, and that retinal ganglion cells differ from hippocampal, cortical, cerebellar, and spinal cord neurons in that bead formation is not blocked by glutamate receptor antagonists, a voltage-gated Na + channel toxin, extracellular Ca 2+ ion exclusion, or temperature shifts. Moreover, we describe a modification of formaldehyde-based fixatives that prevents bead formation in retinal ganglion cells visualized by green fluorescent protein expression and by immunohistochemistry.

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A role for sodium and chloride in kainic acid-induced beading of inhibitory interneuron dendrites

Cited by 53 publications

References 42 publications

Dendritic and Synaptic Pathology in Experimental Autoimmune Encephalomyelitis

Dendritic and Synaptic Pathology in Experimental Autoimmune Encephalomyelitis

Synaptic activity becomes excitotoxic in neurons exposed to elevated levels of platelet-activating factor

Moniliform deformation of retinal ganglion cells by formaldehyde‐based fixatives

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