Circadian control of neural excitability in an animal model of temporal lobe epilepsy

Talathi, Sachin S.; Hwang, Dong‐Uk; Ditto, William L.; Mareci, Thomas H.; Sepulveda, Hector; Spano, Mark L.; Carney, Paul R.

doi:10.1016/j.neulet.2009.03.057

Cited by 33 publications

(51 citation statements)

References 22 publications

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“…As discussed previously, the circadian rhythmic fluctuation observed by Talathi et al suggests that the excitatory and inhibitory spiking activity observed in the CA1 area are driven by an external source (Talathi et al 2009). To simulate these rhythmic fluctuations in the neuronal firing rates, all the neurons in the network considered receive external sinusoidal currents I e (t) and I i (t), which oscillate in-phase to mimic the healthy brain.…”

Section: Spike Ratementioning

confidence: 79%

“…This kind of global modification of the synaptic weights has been used in previous models of HSP (Frohlich et al 2008;Moldakarimov et al 2006) and can be inferred from experimental results seen by Turrigiano and Nelson (2004). As stated earlier, motivated by the results of Talathi et al (2009), we emphasize that our model of HSP assumes the asymptotic synaptic weights, which define the internal set point, to be a function of the phase difference between the oscillating spike rates of the excitatory and inhibitory population.…”

Section: Spike Ratementioning

confidence: 96%

“…1 A schematic of the results seen in Talathi et al (2009). The solid line is representative of the average PS1 spike rate over time, and the dashed line is representative of the average spike rate of PS2 over time.…”

Section: Spike Ratementioning

confidence: 99%

“…Synaptic connections in which the presynaptic neuron is excitatory are shown in red excitatory and inhibitory neurons. Following Talathi et al (2009), we assume that the PS1 represents firing activity of populations of excitatory neurons and PS2 represents firing activity of populations of inhibitory neurons. The network is built using both the spike response neuron model (SRM) (Gerstner and Kistler 2002) and a simple neuron model by Izhikevich (2003) (ISNM) to ensure that the results obtained are independent of the neuronal model used.…”

Section: Spike Ratementioning

confidence: 99%

“…Effects of homeostasis in epilepsy have also been suggested by Talathi et al (2009). The authors monitored firing activity of two classes of population spikes (type 1, labeled as PS1 and type 2, labeled as PS2) following electrically induced brain injury in an animal model of temporal lobe epilepsy.…”

Section: Introductionmentioning

confidence: 99%

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Effects of phase on homeostatic spike rates

et al. 2010

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Recent experimental results by Talathi et al. (Neurosci Lett 455:145-149, 2009) showed a divergence in the spike rates of two types of population spike events, representing the putative activity of the excitatory and inhibitory neurons in the CA1 area of an animal model for temporal lobe epilepsy. The divergence in the spike rate was accompanied by a shift in the phase of oscillations between these spike rates leading to a spontaneous epileptic seizure. In this study, we propose a model of homeostatic synaptic plasticity which assumes that the target spike rate of populations of excitatory and inhibitory neurons in the brain is a function of the phase difference between the excitatory and inhibitory spike rates. With this model of homeostatic synaptic plasticity, we are able to simulate the spike rate dynamics seen experimentally by Talathi et al. in a large network of interacting excitatory and inhibitory neurons using two different spiking neuron models. A drift analysis of the spike rates resulting from the homeostatic synaptic plasticity update rule allowed us to determine the type of synapse that may be primarily involved in the spike rate imbalance in the experimental observation by Talathi et al. We find excitatory neurons, particularly those in which the excitatory neuron is presynaptic, have the most influence in producing the diverging spike rates and causing the spike rates to be anti-phase. Our analysis suggests that the excitatory neuronal population, more specifically the excitatory to excitatory synaptic connections, could be implicated in a methodology designed to control epileptic seizures.

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Section: Spike Ratementioning

confidence: 79%

Section: Spike Ratementioning

confidence: 96%

Section: Spike Ratementioning

confidence: 99%

Section: Spike Ratementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of phase on homeostatic spike rates

et al. 2010

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A Molecular Approach to Epilepsy Management: from Current Therapeutic Methods to Preconditioning Efforts

et al. 2014

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Epilepsy is the most common and chronic neurological disorder characterized by recurrent unprovoked seizures. The key aim in treating patients with epilepsy is the suppression of seizures. An understanding of focal changes that are involved in epileptogenesis may therefore provide novel approaches for optimal treatment of the seizure. Although the actual pathogenesis of epilepsy is still uncertain, recently growing lines of evidence declare that microglia and astrocyte activation, oxidative stress and reactive oxygen species (ROS) production, mitochondria dysfunction, and damage of blood-brain barrier (BBB) are involved in its pathogenesis. Impaired GABAergic function in the brain is probably the most accepted hypothesis regarding the pathogenesis of epilepsy. Clinical neuroimaging of patients and experimental modeling have demonstrated that seizures may induce neuronal apoptosis. Apoptosis signaling pathways are involved in the pathogenesis of several types of epilepsy such as temporal lobe epilepsy (TLE). The quality of life of patients is seriously affected by treatment-related problems and also by unpredictability of epileptic seizures. Moreover, the available antiepileptic drugs (AED) are not significantly effective to prevent epileptogenesis. Thus, novel therapies that are proficient to control seizure in people who are suffering from epilepsy are needed. The preconditioning method promises to serve as an alternative therapeutic approach because this strategy has demonstrated the capability to curtail epileptogenesis. For this reason, understanding of molecular mechanisms underlying brain tolerance induced by preconditioning is crucial to delineate new neuroprotective ways against seizure damage and epileptogenesis. In this review, we summarize the work to date on the pathogenesis of epilepsy and discuss recent therapeutic strategies in the treatment of epilepsy. We will highlight that novel therapy targeting such as preconditioning process holds great promise. In addition, we will also highlight the role of gene reprogramming and mitochondrial biogenesis in the preconditioning-mediated neuroprotective events.

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Neurofibromin Regulates Seizure Attacks in the Rat Pilocarpine-Induced Model of Epilepsy

Ren

Wang

et al. 2015

Mol Neurobiol

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Studies have shown that neurofibromin (NF1) restricts GABA release at inhibitory synapses and regulates dendritic spine formation, which may play an important role in temporal lobe epilepsy (TLE). NF1 expression was detected by double-label immunofluorescence, immunohistochemistry, and western blot analysis in the brains of pilocarpine-induced epilepsy model rats at 6 h, 24 h, 72 h, 7 days, 14 days, 30 days, and 60 days after kindling. NF1 was localized primarily in the nucleus and cytoplasm of neurons. NF1 protein levels significantly increased in the chronic phase (from 7 days until 60 days) in this epileptic rat model. After NF1 expression was knocked down by specific siRNA, the effects of kindling with pilocarpine were evaluated on the 7th day after kindling. The onset latencies of pilocarpine-induced seizures were elevated, and the seizure frequency and duration were reduced in these rats. Our study demonstrates that NF1 promoted seizure attacks in rats with pilocarpine-induced epilepsy.

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Circadian control of neural excitability in an animal model of temporal lobe epilepsy

Cited by 33 publications

References 22 publications

Effects of phase on homeostatic spike rates

Effects of phase on homeostatic spike rates

A Molecular Approach to Epilepsy Management: from Current Therapeutic Methods to Preconditioning Efforts

Neurofibromin Regulates Seizure Attacks in the Rat Pilocarpine-Induced Model of Epilepsy

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