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The pilocarpine model of epilepsy: what have we learned?
Scorza, Fulvio A.;Arida, Ricardo M.;Naffah-Mazzacoratti, Maria da Gra?a;Scerni, Débora A.;Calderazzo, Lineu;Cavalheiro, Esper A.;
Anais da Academia Brasileira de Ciências , 2009, DOI: 10.1590/S0001-37652009000300003
Abstract: the systemic administration of a potent muscarinic agonist pilocarpine in rats promotes sequential behavioral and electrographic changes that can be divided into 3 distinct periods: (a) an acute period that built up progressively into a limbic status epilepticus and that lasts 24 h, (b) a silent period with a progressive normalization of eeg and behavior which varies from 4 to 44 days, and (c) a chronic period with spontaneous recurrent seizures (srss). the main features of the srss observed during the long-term period resemble those of human complex partial seizures and recurs 2-3 times per week per animal. therefore, the pilocarpine model of epilepsy is a valuable tool not only to study the pathogenesis of temporal lobe epilepsy in human condition, but also to evaluate potential antiepileptogenic drugs. this review concentrates on data from pilocarpine model of epilepsy.
Glucose utilisation during status epilepticus in an epilepsy model induced by pilocarpine: a qualitative study
Scorza, Fulvio Alexandre;Arida, Ricardo Mario;Priel, Margareth Rose;Calderazzo, Lineu;Cavalheiro, Esper Abr?o;
Arquivos de Neuro-Psiquiatria , 2002, DOI: 10.1590/S0004-282X2002000200003
Abstract: status epilepticus (se) is a medical emergency and it is associated to brain damage. 2-deoxy-[14c] glucose (2-dg) procedure has been used to measure the alterations in the functional activity of the brain induced by various pharmacological and toxicological agents. the aim of this study was to determine which changes occur in the seizure anatomic substrates during the se induced by pilocarpine (pilo) using [14c]-2 deoxyglucose functional mapping technique. wistar male adult rats were submitted to se pilo-induced for 6h and received [14c] 2-deoxyglucose injection via jugular vein 45 min before the 6th hour of se. the control animals were submitted to all procedures but received saline and not pilocarpine. brain sections were prepared and exposed x-ray film about seven days. the optical density of each region was obtained using a solid state digital analyser. the analysis revealed that 14c-2dg utilisation was pronounced in the se rats on the areas corresponding to the hippocampal formation (+50.6%), caudate-putamen (+30.6%), frontoparietal cortex (+32.2%), amygdala (+31.7%), entorrinal cortex (+28.2%), thalamic nucleus (+93.5%), pre-tectal area (+50.1%) and substantia nigra (+50.3%) when compared to control. our results suggest that the different activation levels of the distinct structures may be particularly important for understanding triggering and spreading mechanisms underlying epileptic activity during status epilepticus.
Glucose utilisation during status epilepticus in an epilepsy model induced by pilocarpine: a qualitative study  [cached]
Scorza Fulvio Alexandre,Arida Ricardo Mario,Priel Margareth Rose,Calderazzo Lineu
Arquivos de Neuro-Psiquiatria , 2002,
Abstract: Status epilepticus (SE) is a medical emergency and it is associated to brain damage. 2-deoxy-[14C] glucose (2-DG) procedure has been used to measure the alterations in the functional activity of the brain induced by various pharmacological and toxicological agents. The aim of this study was to determine which changes occur in the seizure anatomic substrates during the SE induced by pilocarpine (PILO) using [14C]-2 deoxyglucose functional mapping technique. Wistar male adult rats were submitted to SE PILO-induced for 6h and received [14C] 2-deoxyglucose injection via jugular vein 45 min before the 6th hour of SE. The control animals were submitted to all procedures but received saline and not pilocarpine. Brain sections were prepared and exposed X-ray film about seven days. The optical density of each region was obtained using a solid state digital analyser. The analysis revealed that 14C-2DG utilisation was pronounced in the SE rats on the areas corresponding to the hippocampal formation (+50.6%), caudate-putamen (+30.6%), frontoparietal cortex (+32.2%), amygdala (+31.7%), entorrinal cortex (+28.2%), thalamic nucleus (+93.5%), pre-tectal area (+50.1%) and substantia nigra (+50.3%) when compared to control. Our results suggest that the different activation levels of the distinct structures may be particularly important for understanding triggering and spreading mechanisms underlying epileptic activity during status epilepticus.
Hippocampal Desynchronization of Functional Connectivity Prior to the Onset of Status Epilepticus in Pilocarpine-Treated Rats  [PDF]
Chi-Han Wang, Chou P. Hung, Ming-Teh Chen, Yang-Hsin Shih, Yung-Yang Lin
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0039763
Abstract: Status epilepticus (SE), a pro-epileptogenic brain insult in rodent models of temporal lobe epilepsy, is successfully induced by pilocarpine in some, but not all, rats. This study aimed to identify characteristic alterations within the hippocampal neural network prior to the onset of SE. Sixteen microwire electrodes were implanted into the left hippocampus of male Sprague-Dawley rats. After a 7-day recovery period, animal behavior, hippocampal neuronal ensemble activities, and local field potentials (LFP) were recorded before and after an intra-peritoneal injection of pilocarpine (350 mg/kg). The single-neuron firing, population neuronal correlation, and coincident firing between neurons were compared between SE (n = 9) and nonSE rats (n = 12). A significant decrease in the strength of functional connectivity prior to the onset of SE, as measured by changes in coincident spike timing between pairs of hippocampal neurons, was exclusively found in SE rats. However, single-neuron firing and LFP profiles did not show a significant difference between SE and nonSE rats. These results suggest that desynchronization in the functional circuitry of the hippocampus, likely associated with a change in synaptic strength, may serve as an electrophysiological marker prior to SE in pilocarpine-treated rats.
Alterations of the electroencephalogram sub-bands amplitude during focal seizures in the pilocarpine model of epilepsy
Sahel Motaghi,Mohammad Niknazar,Mohammad Sayyah,Vahab Babapour
Physiology and Pharmacology , 2012,
Abstract: Introduction: Temporal lobe epilepsy (TLE) is the most common and drug resistant epilepsy in adults. Due to behavioral, morphologic and electrographic similarities, pilocarpine model of epilepsy best resembles TLE. This study was aimed at determination of the changes in electroencephalogram (EEG) sub-bands amplitude during focal seizures in the pilocarpine model of epilepsy. Analysis of these changes might help detection of a pre-seizure state before an oncoming seizure. Methods: Rats were treated by scopolamine (1mg/kg, s.c) to prevent cholinergic effects. After 30 min, pilocarpine (380 mg/kg, i.p) was administered to induce status epilepticus (SE) and 2 hours after SE, diazepam (20 mg/kg, i.p) was injected to suppress the seizures. EEG was recorded in the epileptic rats by superficial electrodes. EEG signal in each rat was decomposed to its sub-bands alpha, beta, gamma, theta and delta by Daubechies wavelet transform. The power (square of amplitude) of sub-band during focal seizures was compared with the same sub-band in pre-ictal stage and the percent of changes in each rat was calculated. Results: SE occurred in 65% of the animals and happened 39.4±5.4 min after injection of pilocarpine. Focal and generalized seizures were developed 3.8±0.4 and 7.0±0.5 days after SE, respectively. Although power of EEG and its sub-bands decreased during focal seizures, the changes were not statistically significant. The greatest decrease in power pertained to beta and gamma sub-bands, while alpha and theta sub-bands underwent the least changes. Conclusion: Based on the protocol used in this study, it seems that the power of EEG sub-bands does not change during focal seizures in pilocarpine model of epilepsy.
Absence-like seizures in adult rats following pilocarpine-induced status epilepticus early in life
Ferreira, B.L.C.;Valle, A.C.;Cavalheiro, E.A.;Timo-Iaria, C.;
Brazilian Journal of Medical and Biological Research , 2003, DOI: 10.1590/S0100-879X2003001200010
Abstract: administration of pilocarpine causes epilepsy in rats if status epilepticus (se) is induced at an early age. to determine in detail the electrophysiological patterns of the epileptogenic activity in these animals, 46 wistar rats, 7-17 days old, were subjected to se induced by pilocarpine and electro-oscillograms from the cortex, hippocampus, amygdala, thalamus and hypothalamus, as well as head, rostrum and vibrissa, eye, ear and forelimb movements, were recorded 120 days later. six control animals of the same age range did not show any signs of epilepsy. in all the rats subjected to se, iterative spike-wave complexes (8.1 ± 0.5 hz in frequency, 18.9 ± 9.1 s in duration) were recorded from the frontal cortex during absence fits. however, similar spike-wave discharges were always found also in the hippocampus and, less frequently, in the amygdala and in thalamic nuclei. repetitive or single spikes were also detected in these same central structures. clonic movements and single jerks were recorded from all the rats, either concomitantly with or independently of the spike-wave complexes and spikes. we conclude that rats made epileptic with pilocarpine develop absence seizures also occurring during paradoxical sleep, showing the characteristic spike-wave bursts in neocortical areas and also in the hippocampus. this is in contrast to the well-accepted statement that one of the main characteristics of absence-like fits in the rat is that spike-wave discharges are never recorded from the hippocampal fields.
Absence-like seizures in adult rats following pilocarpine-induced status epilepticus early in life  [cached]
Ferreira B.L.C.,Valle A.C.,Cavalheiro E.A.,Timo-Iaria C.
Brazilian Journal of Medical and Biological Research , 2003,
Abstract: Administration of pilocarpine causes epilepsy in rats if status epilepticus (SE) is induced at an early age. To determine in detail the electrophysiological patterns of the epileptogenic activity in these animals, 46 Wistar rats, 7-17 days old, were subjected to SE induced by pilocarpine and electro-oscillograms from the cortex, hippocampus, amygdala, thalamus and hypothalamus, as well as head, rostrum and vibrissa, eye, ear and forelimb movements, were recorded 120 days later. Six control animals of the same age range did not show any signs of epilepsy. In all the rats subjected to SE, iterative spike-wave complexes (8.1 ± 0.5 Hz in frequency, 18.9 ± 9.1 s in duration) were recorded from the frontal cortex during absence fits. However, similar spike-wave discharges were always found also in the hippocampus and, less frequently, in the amygdala and in thalamic nuclei. Repetitive or single spikes were also detected in these same central structures. Clonic movements and single jerks were recorded from all the rats, either concomitantly with or independently of the spike-wave complexes and spikes. We conclude that rats made epileptic with pilocarpine develop absence seizures also occurring during paradoxical sleep, showing the characteristic spike-wave bursts in neocortical areas and also in the hippocampus. This is in contrast to the well-accepted statement that one of the main characteristics of absence-like fits in the rat is that spike-wave discharges are never recorded from the hippocampal fields.
Optogenetic Delay of Status Epilepticus Onset in an In Vivo Rodent Epilepsy Model  [PDF]
Inna Sukhotinsky, Alexander M. Chan, Omar J. Ahmed, Vikram R. Rao, Viviana Gradinaru, Charu Ramakrishnan, Karl Deisseroth, Ania K. Majewska, Sydney S. Cash
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0062013
Abstract: Epilepsy is a devastating disease, currently treated with medications, surgery or electrical stimulation. None of these approaches is totally effective and our ability to control seizures remains limited and complicated by frequent side effects. The emerging revolutionary technique of optogenetics enables manipulation of the activity of specific neuronal populations in vivo with exquisite spatiotemporal resolution using light. We used optogenetic approaches to test the role of hippocampal excitatory neurons in the lithium-pilocarpine model of acute elicited seizures in awake behaving rats. Hippocampal pyramidal neurons were transduced in vivo with a virus carrying an enhanced halorhodopsin (eNpHR), a yellow light activated chloride pump, and acute seizure progression was then monitored behaviorally and electrophysiologically in the presence and absence of illumination delivered via an optical fiber. Inhibition of those neurons with illumination prior to seizure onset significantly delayed electrographic and behavioral initiation of status epilepticus, and altered the dynamics of ictal activity development. These results reveal an essential role of hippocampal excitatory neurons in this model of ictogenesis and illustrate the power of optogenetic approaches for elucidation of seizure mechanisms. This early success in controlling seizures also suggests future therapeutic avenues.
Gabapentin Administration Reduces Reactive Gliosis and Neurodegeneration after Pilocarpine-Induced Status Epilepticus  [PDF]
Alicia Raquel Rossi, Maria Florencia Angelo, Alejandro Villarreal, Jerónimo Lukin, Alberto Javier Ramos
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0078516
Abstract: The lithium-pilocarpine model of epilepsy reproduces in rodents several features of human temporal lobe epilepsy, by inducing an acute status epilepticus (SE) followed by a latency period. It has been proposed that the neuronal network reorganization that occurs during latency determines the subsequent appearance of spontaneous recurrent seizures. The aim of this study was to evaluate neuronal and glial responses during the latency period that follows SE. Given the potential role of astrocytes in the post-SE network reorganization, through the secretion of synaptogenic molecules such as thrombospondins, we also studied the effect of treatment with the α2δ1 thrombospondin receptor antagonist gabapentin. Adult male Wistar rats received 3 mEq/kg LiCl, and 20 h later 30 mg/kg pilocarpine. Once SE was achieved, seizures were stopped with 20 mg/kg diazepam. Animals then received 400 mg/kg/day gabapentin or saline for either 4 or 14 days. In vitro experiments were performed in dissociated mixed hippocampal cell culture exposed to glutamate, and subsequently treated with gabapentin or vehicle. During the latency period, the hippocampus and pyriform cortex of SE-animals presented a profuse reactive astrogliosis, with increased GFAP and nestin expression. Gliosis intensity was dependent on the Racine stage attained by the animals and peaked 15 days after SE. Microglia was also reactive after SE, and followed the same pattern. Neuronal degeneration was present in SE-animals, and also depended on the Racine stage and the SE duration. Polysialic-acid NCAM (PSA-NCAM) expression was increased in hippocampal CA-1 and dentate gyrus of SE-animals. Gabapentin treatment was able to reduce reactive gliosis, decrease neuronal loss and normalize PSA-NCAM staining in hippocampal CA-1. In vitro, gabapentin treatment partially prevented the dendritic loss and reactive gliosis caused by glutamate excitotoxicity. Our results show that gabapentin treatment during the latency period after SE protects neurons and normalizes PSA-NCAM probably by direct interaction with neurons and glia.
MicroRNA expression profile of the hippocampus in a rat model of temporal lobe epilepsy and miR-34a-targeted neuroprotection against hippocampal neurone cell apoptosis post-status epilepticus  [cached]
Hu Kai,Xie Yuan-Yuan,Zhang Chen,Ouyang Dong-Sheng
BMC Neuroscience , 2012, DOI: 10.1186/1471-2202-13-115
Abstract: Background The expression pattern and function of miRNAs in the rat model of temporal lobe epilepsy have not been well defined. Profiling miRNA expression in the rat model of temporal lobe epilepsy and investigating the function of specific miRNAs in epilepsy offers the prospect of a deeper understanding of the mechanisms of epilepsy. Methods The lithium-pilocarpine-induced status epilepticus model and the temporal lobe epilepsy model were established in Sprague–Dawley rats. Samples were analysed to detect deregulated miRNAs in the hippocampal temporal lobe, and several of these deregulated miRNAs were confirmed by qPCR. The expression of the pro-apoptotic miR-34a was detected at 1 day, 7 days and 2 weeks post-status epilepticus and at 2 months after temporal lobe epilepsy. The antagomir of miR-34a was then utilised. The expression of miR-34a after targeting and the expression change of activated caspase-3 protein were examined. The effects of altering the expression of miR-34a and activated caspase-3 protein on neuronal survival and neuronal death or apoptosis post-status epilepticus were assessed. Results The miRNA microarray detected 9 up-regulated miRNAs (miR-146a, -211, -203, -210, -152, -31, -23a, -34a, -27a) and 15 down-regulated miRNAs (miR-138*, -301a, -136, -153, -19a, -135b, -325-5p, -380, -190, -542-3p, -33, -144, -542-5p, -543, -296*). Some of the deregulated miRNAs (miR-146a, miR-210, miR-27a, miR-135b and miR-33) were confirmed using qPCR. Furthermore, an increase in expression of the pro-apoptotic miR-34a was demonstrated in the post-status epilepticus rat hippocampus. miR-34a was significantly up-regulated at 1 day, 7 days and 2 weeks post-status epilepticus and at 2 months after temporal lobe epilepsy. Experiments with the miR-34a antagomir revealed that targeting miR-34a led to an inhibition of activated caspase-3 protein expression, which may contribute to increased neuronal survival and reduced neuronal death or apoptosis. Conclusions Our study showed the expression profile of miRNAs in the hippocampus in a rat model of temporal lobe epilepsy and an increase in the expression of the pro-apoptotic miR-34a in post-status epilepticus rats. The results show that miR-34a is up-regulated during seizure-induced neuronal death or apoptosis, and targeting miR-34a is neuroprotective and is associated with an inhibition of an increase in activated caspase-3 protein.
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