The contribution of the lateral posterior and anteroventral thalamic nuclei on spontaneous recurrent seizures in the pilocarpine model of epilepsy

Arida, Ricardo Mário; Priel, Margareth Rose; Calderazzo, Lineu; Cavalheiro, Ésper Abrão

doi:10.1590/s0004-282x2002000400011

Cited by 21 publications

(20 citation statements)

References 11 publications

(13 reference statements)

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“…Indeed, we found that over 46% of the CTZ rats (6 out of 13) had recurrent seizure with the latency between 2 weeks to 6 months. The silent period between acute seizure induction and the occurrence of the recurrent seizure in this CTZ seizure rat model seems well in agreement with the other classic seizure animal model, at around two-week time of latency, such as pilocarpine and Kainic acid induced seizure models [24, 25]. However, the rate of the animal to have recurrent seizure seems lower than other seizure models.…”

Section: Discussionsupporting

confidence: 85%

“…Although we have demonstrated that CTZ induced seizure in freely moving rats [12], a successful seizure animal model requires the animals to develop recurrent seizure and also have a high proportion to have recurrent seizure [24]. In this aspect we carried out the current study to investigate whether the acutely induced seizure rats by CTZ could develop to have recurrent seizure.…”

Section: Discussionmentioning

confidence: 99%

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Downregulated GABA and BDNF-TrkB Pathway in Chronic Cyclothiazide Seizure Model

et al. 2014

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Cyclothiazide (CTZ) has been reported to simultaneously enhance glutamate receptor excitation and inhibit GABAA receptor inhibition, and in turn it evokes epileptiform activities in hippocampal neurons. It has also been shown to acutely induce epileptic seizure behavior in freely moving rats. However, whether CTZ induced seizure rats could develop to have recurrent seizure still remains unknown. In the current study, we demonstrated that 46% of the CTZ induced seizure rats developed to have recurrent seizure behavior as well as epileptic EEG with a starting latency between 2 weeks and several months. In those chronic seizure rats 6 months after the seizure induction by the CTZ, our immunohistochemistry results showed that both GAD and GAT-1 were significantly decreased across CA1, CA3, and dentate gyrus area of the hippocampus studied. In addition, both BDNF and its receptor TrkB were also decreased in hippocampus of the chronic CTZ seizure rats. Our results indicate that CTZ induced seizure is capable of developing to have recurrent seizure, and the decreased GABA synthesis and transport as well as the impaired BDNF-TrkB signaling pathway may contribute to the development of the recurrent seizure. Thus, CTZ seizure rats may provide a novel animal model for epilepsy study and anticonvulsant drug testing in the future.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Downregulated GABA and BDNF-TrkB Pathway in Chronic Cyclothiazide Seizure Model

et al. 2014

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“…As our AN lesions compromised a large volume of tissue (most of anteroventral thalamic nucleus and parts of the anterodorsal and anteromedial nuclei), they have likely also injured fibers from the mammillothalamic tract and efferents from the AN to the cingulum. Similar to our results however, Scorza et al [22] using chemical ablation with ibotenic acid (supposedly harmful only to neurons), have shown that lesions in parts of the anteroventral nucleus did not alter the frequency of spontaneous seizures in pilocarpine epileptic rats. Results from our study and the one by Scorza et al suggest that, independent on the extent of the lesion or the method used for their production, AN thalamotomies are not protective against SRS in chronic pilocarpine epileptic rats.…”

Section: Discussionsupporting

confidence: 92%

Bilateral Anterior Thalamic Nucleus Lesions Are Not Protective against Seizures in Chronic Pilocarpine Epileptic Rats

Hamani

Ewerton

Almeida

et al. 2009

Stereotact Funct Neurosurg

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Aims: To investigate whether anterior thalamic nucleus (AN) lesions are protective against spontaneous recurrent seizures in the chronic phase of the pilocarpine model of epilepsy. Methods: Two groups of rats were treated with bilateral AN radiofrequency thalamotomies or sham surgery 2 weeks after pilocarpine-induced status epilepticus. After the lesions, animals were videotaped from the 2nd to the 8th week after status epilepticus (total 180 h). Results: During the 6 weeks of observation, no differences in the frequency of spontaneous seizures were found between animals that had bilateral AN lesions (n = 26; 3.1 ± 0.6 seizures per animal) and controls (n = 25; 3.0 ± 0.6 seizures per animal; p = 0.8). Conclusions: We conclude that AN thalamotomies were not effective in reducing the frequency of seizures during the chronic phase of the pilocarpine model of epilepsy.

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“…Before these studies are undertaken, it is prudent for us to clarify our research background. In a previous study, our research group found that the thalamus plays an interesting and important role in the cerebral circuits of rats with epilepsy67,68. Interestingly, in studies of epilepsy, which is the most prevalent serious neurological condition worldwide, clinical data suggest that these patients are at a two- to threefold higher risk of dying prematurely than those without epilepsy.…”

Section: Thalamic Nuclear Abnormalities and Sudden Cardiac Death In Smentioning

confidence: 90%

Thalamic nuclear abnormalities as a contributory factor in sudden cardiac deaths among patients with schizophrenia

Schmitt

Cysneiros

Arida

et al. 2010

Clinics

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Patients with schizophrenia have a two- to three-fold increased risk of premature death as compared to patients without this disease. It has been established that patients with schizophrenia are at a high risk of developing cardiovascular disease. Moreover, an important issue that has not yet been explored is a possible existence of a “cerebral” focus that could trigger sudden cardiac death in patients with schizophrenia. Along these lines, several structural and functional alterations in the thalamic complex are evident in patients with schizophrenia and have been correlated with the symptoms manifested by these patients. With regard to abnormalities on the cellular and molecular level, previous studies have shown that schizophrenic patients have fewer neuronal projections from the thalamus to the prefrontal cortex as well as a reduced number of neurons, a reduced volume of either the entire thalamus or its subnuclei, and abnormal glutamate signaling. According to the glutamate hypothesis of schizophrenia, hypofunctional corticostriatal and striatothalamic projections are directly involved in the pathophysiology of the disease. Animal and post-mortem studies have provided a large amount of evidence that links the sudden unexpected death in epilepsy (SUDEP) that occurs in patients with schizophrenia and epilepsy to thalamic changes. Based on the results of these prior studies, it is clear that further research regarding the relationship between the thalamus and sudden cardiac death is of vital importance.

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The contribution of the lateral posterior and anteroventral thalamic nuclei on spontaneous recurrent seizures in the pilocarpine model of epilepsy

Cited by 21 publications

References 11 publications

Downregulated GABA and BDNF-TrkB Pathway in Chronic Cyclothiazide Seizure Model

Downregulated GABA and BDNF-TrkB Pathway in Chronic Cyclothiazide Seizure Model

Bilateral Anterior Thalamic Nucleus Lesions Are Not Protective against Seizures in Chronic Pilocarpine Epileptic Rats

Thalamic nuclear abnormalities as a contributory factor in sudden cardiac deaths among patients with schizophrenia

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