Ultrastructural changes to rat hippocampus in pentylenetetrazol- and kainic acid-induced status epilepticus: A study using electron microscopy

Deformation of Mitochondrial Cristae in Human Neural Progenitor Cells Exposed to Valproic Acid

“…Furthermore, mitochondrial dysfunction is commonly associated to neuropsychiatric disorders due to defects in neurotransmitter release and cell redox signaling (Arun et al 2016, Tait andGreen 2012). In addition, ultrastructural analysis of rats' hippocampus in pentylenetetrazol (PTZ)-induced status epilepticus showed alterations in mitochondrial morphology, suggesting a dysfunction related to epileptic pathophysiology (Zhvania et al 2015). RODRIGO M. DA COSTA, KARINA KARMIRIAN and STEVENS K. REHEN In 1882, valproic acid (VPA) was first described as an organic solvent.…”

Brain Hyperstimulation by Epileptic Seizures

“…As a result of this binding there is a depression of the action of inhibitory neurotransmitters (mainly GABA) making the system hyperexcitable. 6 Excess neuronal excitation can corrupt cellular function, osmotic damage results in chloride inflow that brings water into the cell. In these cases, there may be excessive calcium influx which thus not only mediates gene expression but also activates proteases and lipases and can cause cell death.…”

“…In these cases, there may be excessive calcium influx which thus not only mediates gene expression but also activates proteases and lipases and can cause cell death. 6 In the scientific community there are 3 main models with PTZ:1-single administration of convulsive dose; 2-kindling, caused by repeated subvulsive doses over time (usually days) and 3 -application of several low (but convulsive) doses with intervals without crisis. The three models cause short-term epileptic seizures and, initially, they present with absence of neuronal degeneration.…”

“…The three models cause short-term epileptic seizures and, initially, they present with absence of neuronal degeneration. Therefore, the use of PTZ is indicated to study mechanisms of early cellular responses, induced by epileptic seizures and that develop, at first, independently of neuronal death 6 . Repeated treatment with PTZ causes structural changes mainly in pyramidal cells and interneurons.…”

“…4 Disappearance of dendritic microtubules, breakdown of cytoskeletal elements (among them actin) and decrease in the number of dendritic spines are also structural alterations following PTZ-induced seizures. 6 Cellular responses of recurrent epileptic seizures through PTZ involve inflammation (vasodilation and perivascular proliferation of leukocytes), neurogenesis and reactive glioses in different animal species, including zebrafish, rodents and primates. However, evidence of epileptogenesis (only after numerous seizures with PTZ) was only found in rodents and primates, probably because of the high regeneration capacity found in zebrafish brain.…”