Time-course of neuronal death in the mouse pilocarpine model of chronic epilepsy using Fluoro-Jade C staining

Lian, Wang; Yong-hong, Liu; Huang, Yuan-Gui; Chen, Liang-Wei

doi:10.1016/j.brainres.2008.07.097

Cited by 94 publications

(110 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…3) was observed in the hippocampus shortly after (on day 4) pilocarpine-induced SE. These signs of hippocampal damage (neurodegeneration and reactive gliosis) have also been reported to show up a few hours after SE (Rossi et al 2013;Wang et al 2008). Unlike glucose metabolism, these brain damage markers remain longer, as they were even detectable 33 days following the SE (Shiha et al 2015).…”

Section: Discussionmentioning

confidence: 90%

“…hil hilus, dg dentate gyrus. Scale bar 250 lm Cell Mol Neurobiol amygdala, striatum, and septum (Rossi et al 2013;Wang et al 2008). Subacute fluoxetine administration prevented the brain metabolic impairment and reduced damage signs induced by lithium-pilocarpine (Shiha et al 2015).…”

Section: Discussionmentioning

confidence: 99%

“…It is characterized by a rapid status epilepticus (SE) followed by a latent period in which generalized brain hypometabolism (Goffin et al 2009;Guo et al 2009;Lee et al 2012) and neuronal damage (primarily in hippocampus) appear (Mello et al 1993;Rossi et al 2013;Wang et al 2008). Brain hypometabolism has been described to appear shortly after the SE onset, returning the metabolic activity to baseline values in the subacute period (Lee et al 2012).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Serotonin Depletion Does not Modify the Short-Term Brain Hypometabolism and Hippocampal Neurodegeneration Induced by the Lithium–Pilocarpine Model of Status Epilepticus in Rats

et al. 2015

View full text Add to dashboard Cite

It has been reported that fluoxetine, a selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitor, has neuroprotective properties in the lithium-pilocarpine model of status epilepticus (SE) in rats. The aim of the present study was to investigate the effect of 5-HT depletion by short-term administration of p-chlorophenylalanine (PCPA), a specific tryptophan hydroxylase inhibitor, on the brain hypometabolism and neurodegeneration induced in the acute phase of this SE model. Our results show that 5-HT depletion did modify neither the brain basal metabolic activity nor the lithium-pilocarpine-induced hypometabolism when evaluated 3 days after the insult. In addition, hippocampal neurodegeneration and astrogliosis triggered by lithium-pilocarpine were not exacerbated by PCPA treatment. These findings point out that in the early latent phase of epileptogenesis, non-5-HT-mediated actions may contribute, at least in some extent, to the neuroprotective effects of fluoxetine in this model of SE.

show abstract

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Serotonin Depletion Does not Modify the Short-Term Brain Hypometabolism and Hippocampal Neurodegeneration Induced by the Lithium–Pilocarpine Model of Status Epilepticus in Rats

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Pilocarpine-induced status epilepticus causes neuronal death in the rodent brain (Benkovic, O'Callaghan et al 2004;Wang, Liu et al 2008). Pilocarpine is a muscarinic agonist which activates M1 muscarinic receptors directly.…”

Section: Discussionmentioning

confidence: 99%

“…The reason to choose Fluoro-Jade C is because it has much stronger affinity for degenerating neurons than Fluoro-Jade B and it stains with "highest resolution" (Schmued, Stowers et al 2005). Fluoro-Jade C stains all dead neurons no matter whether it had died by apoptosis or necrosis (Wang, Liu et al 2008). The exact mechanism by which this stain binds with degenerating neurons is still not clear.…”

Section: Discussionmentioning

confidence: 99%

Silencing Hyper-Excitable Neurons as a Treatment for Status Epilepticus and Temporal Lobe Epilepsy.

Dey¹

View full text Add to dashboard Cite

Blockade of excitatory synaptogenesis with proximal dendrites of dentate granule cells following rapamycin treatment in a mouse model of temporal lobe epilepsy

Yamawaki

Thind²,

Buckmaster³

2014

J of Comparative Neurology

View full text Add to dashboard Cite

Inhibiting the mTOR signaling pathway with rapamycin blocks granule cell axon (mossy fiber) sprouting after epileptogenic injuries, including pilocarpine-induced status epilepticus. However, it remains unclear whether axons from other types of neurons sprout into the inner molecular layer and synapse with granule cell dendrites despite rapamycin treatment. If so, other aberrant positive-feedback networks might develop. To test this possibility stereological electron microscopy was used to estimate numbers of excitatory synapses in the inner molecular layer per hippocampus in pilocarpine-treated control mice, in mice 5 d after pilocarpine-induced status epilepticus, and after status epilepticus and daily treatment beginning 24 h later with rapamycin or vehicle for 2 months. The optical fractionator method was used to estimate numbers of granule cells in Nissl-stained sections so that numbers of excitatory synapses in the inner molecular layer per granule cell could be calculated. Control mice had an average of 2280 asymmetric synapses in the inner molecular layer per granule cell, which was reduced to 63% of controls 5 d after status epilepticus, recovered to 93% of controls in vehicle-treated mice 2 months after status epilepticus, but remained at only 63% of controls in rapamycin-treated mice. These findings reveal that rapamycin prevented excitatory axons from synapsing with proximal dendrites of granule cells and raise questions about the recurrent excitation hypothesis of temporal lobe epilepsy.

show abstract

Time-course of neuronal death in the mouse pilocarpine model of chronic epilepsy using Fluoro-Jade C staining

Cited by 94 publications

References 46 publications

Serotonin Depletion Does not Modify the Short-Term Brain Hypometabolism and Hippocampal Neurodegeneration Induced by the Lithium–Pilocarpine Model of Status Epilepticus in Rats

Serotonin Depletion Does not Modify the Short-Term Brain Hypometabolism and Hippocampal Neurodegeneration Induced by the Lithium–Pilocarpine Model of Status Epilepticus in Rats

Silencing Hyper-Excitable Neurons as a Treatment for Status Epilepticus and Temporal Lobe Epilepsy.

Blockade of excitatory synaptogenesis with proximal dendrites of dentate granule cells following rapamycin treatment in a mouse model of temporal lobe epilepsy

Contact Info

Product

Resources

About