scholarly journals Diurnal Burden of Spontaneous Seizures in Early Epileptogenesis in the Post‐Kainic Acid Rat Model of Epilepsy

2021 ◽  
Author(s):  
Stephanie Mizuno ◽  
Zachery Koneval ◽  
Dannielle K. Zierath ◽  
Kevin M. Knox ◽  
H. Steve White ◽  
...  
Keyword(s):  
Kainic Acid ◽  
Rat Model ◽  
Spontaneous Seizures

scholarly journals Dynamic structural neuroplasticity during and after epileptogenesis in a pilocarpine rat model of epilepsy

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Soomaayeh Heysieattalab ◽  
Leila Sadeghi
Keyword(s):  
Rat Model ◽  
Chronic Phase ◽  
Structural Plasticity ◽  
Epileptic Seizures ◽  
Experimental Models ◽  
Spontaneous Seizures ◽  
Maladaptive Plasticity ◽  
Male Wistar Rats ◽  
Spontaneous Recurrent Seizures ◽  
Latent Phase

Abstract Background The role of neuroplasticity in epilepsy has been widely studied in experimental models and human brain samples. However, the results are contradictory and it remains unclear if neuroplasticity is more related to the cause or the consequence of epileptic seizures. Clarifying this issue can provide insights into epilepsy therapies that target the disease mechanism and etiology rather than symptoms. Therefore, this study was aimed to investigate the dynamic changes of structural plasticity in a pilocarpine rat model of epilepsy. Methods A single acute dose of pilocarpine (380 mg/kg, i.p.) was injected into adult male Wistar rats to induce status epilepticus (SE). Animal behavior was monitored for 2 h. Immunohistochemical staining was performed to evaluate neurogenesis in the CA3 and dentate gyrus (DG) regions of hippocampus using biomarkers Ki67 and doublecortin (DCX). The Golgi-Cox method was performed to analyze dendritic length and complexity. All experiments were performed in control rats (baseline), at 24 h after SE, on day 20 after SE (latent phase), after the first and 10th spontaneous recurrent seizures (SRS; chronic phase), and in non-epileptic rats (which did not manifest SRS 36 days after pilocarpine injection). Results SE significantly increased the number of Ki67 and DCX-positive cells, suggesting neurogenesis during the latent phase. The dendritic complexity monitoring showed that plasticity was altered differently during epilepsy and epileptogenesis, suggesting that the two processes are completely separate at molecular and physiological levels. The numbers of spines and mushroom-type spines were increased in the latent phase. However, the dendritogenesis and spine numbers did not increase in rats that were unable to manifest spontaneous seizures after SE. Conclusion All parameters of structural plasticity that increase during epileptogenesis, are reduced by spontaneous seizure occurrence, which suggests that the development of epilepsy involves maladaptive plastic changes. Therefore, the maladaptive plasticity biomarkers can be used to predict epilepsy before development of SRS in the cases of serious brain injury.

scholarly journals Effects of Circadian Regulation and Rest-Activity State on Spontaneous Seizures in a Rat Model of Limbic Epilepsy

Epilepsia ◽  
2000 ◽  
Vol 41 (5) ◽  
pp. 502-509 ◽  
Author(s):  
Mark Quigg ◽  
Hope Clayburn ◽  
Martin Straume ◽  
Michael Menaker ◽  
Edward H. Bertram
Keyword(s):  
Rat Model ◽  
Circadian Regulation ◽  
Spontaneous Seizures ◽  
Activity State ◽  
Rest Activity

Pancreatitis-associated protein-I and pancreatitis-associated protein-III expression in a rat model of kainic acid-induced seizure

Neuroscience ◽  
2011 ◽  
Vol 175 ◽  
pp. 273-280 ◽  
Author(s):  
S. Kawahara ◽  
H. Konishi ◽  
M. Morino ◽  
K. Ohata ◽  
H. Kiyama
Keyword(s):  
Kainic Acid ◽  
Rat Model ◽  
Pancreatitis Associated Protein

scholarly journals Heterozygous deletion of SYNGAP enzymatic domains in rats causes selective learning, social and seizure phenotypes

2020 ◽  
Author(s):  
D. Katsanevaki ◽  
SM. Till ◽  
I. Buller-Peralta ◽  
TC. Watson ◽  
MS. Nawaz ◽  
...  
Keyword(s):  
Rat Model ◽  
Brain Function ◽  
Autism Spectrum ◽  
Lipid Binding ◽  
Normal Brain ◽  
Heterozygous Deletion ◽  
Pathogenic Variants ◽  
Spontaneous Seizures ◽  
Normal Brain Function ◽  
Intrinsic Gtpase Activity

AbstractPathogenic variants in SYNGAP1 are one of the most common genetic causes of nonsyndromic intellectual disability (ID) and are considered a risk for autism spectrum disorder (ASD). SYNGAP1 encodes a synaptic GTPase activating protein that modulates the intrinsic GTPase activity of several small G-proteins and is implicated in regulating the composition of the postsynaptic density. By targeting the deletion of exons encoding the calcium/lipid binding (C2) and GTPase activating protein (GAP) domains, we generated a novel rat model to study SYNGAP related pathophysiology. We find that rats heterozygous for the C2/GAP domain deletion (Syngap+/Δ-GAP) exhibit reduced exploration and fear extinction, altered social behaviour, and spontaneous seizures, while homozygous mutants die within days after birth. This new rat model reveals that the enzymatic domains of SYNGAP are essential for normal brain function and provide an important new model system in the study of both ID/ASD and epilepsy.

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