Detailed spectral profile analysis of penicillin-induced epileptiform activity in anesthetized rats

Canan, Sinan; Ankaralı, Seyit; Marangoz, C.

doi:10.1016/j.eplepsyres.2008.06.005

Cited by 18 publications

(7 citation statements)

References 23 publications

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“…The increase in power induced by PG in all bands was responsible for disinhibition of synchronous firing activity in the cortex, consistent with previous studies (Canan et al, 2008; Kida et al, 2012). An in vivo study showed that all bands (delta, theta, alpha, beta 1, and beta 2) in the power density spectra of PG-induced EDs were suppressed by FCC to 15°C (Kida et al, 2012), a temperature at which the TRPM8 channel is activated (Peier et al, 2002).…”

Section: Discussionsupporting

confidence: 92%

Suppressive Effects of Cooling Compounds Icilin on Penicillin G-Induced Epileptiform Discharges in Anesthetized Rats

et al. 2019

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More than 30% of patients with epilepsy are refractory and have inadequate seizure control. Focal cortical cooling (FCC) suppresses epileptiform discharges (EDs) in patients with refractory focal cortical epilepsy. However, little is known about the mechanism by which FCC inhibits seizures at 15°C, and FCC treatment is highly invasive. Therefore, new antiepileptic drugs are needed that produce the same effects as FCC but with different mechanisms of action. To address this need, we focused on transient receptor potential melastatin 8 (TRPM8), an ion channel that detects cold, which is activated at 15°C. We examined whether TRPM8 activation suppresses penicillin G (PG)-induced EDs in anesthetized rats. Icilin, a TRPM8 and TRP Ankyrin 1 agonist, was administered after PG injection, and a focal electrocorticogram (ECoG) and cortical temperature were recorded for 4 h. We measured spike amplitude, duration, firing rate, and power density in each band to evaluate the effects of icilin. PG-induced EDs and increased delta, theta, alpha, and beta power spectra were observed in the ECoG. Icilin suppressed EDs while maintaining cortical temperature. In particular, 3.0-mM icilin significantly suppressed PG-induced spike amplitude, duration, and firing rate and improved the increased power density of each band in the EDs to the level of basal activity in the ECoG. These suppressive effects of 3.0-mM icilin on EDs were antagonized by administering N-(3-aminopropyl)-2-[(3-methylphenyl) methoxy]-N-(2-thienylmethyl)-benzamide hydrochloride (AMTB), a selective TRPM8 inhibitor. Our results suggest that TRPM8 activation in epileptic brain regions may be a new therapeutic approach for patients with epilepsy.

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Section: Discussionsupporting

confidence: 92%

Suppressive Effects of Cooling Compounds Icilin on Penicillin G-Induced Epileptiform Discharges in Anesthetized Rats

et al. 2019

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“…Alternatively, we can keep G FIN in physiological range [40.0, 60.0] mV but would entail that the number of synaptic connections from fast interneurons to pyramidal cells is twice than the standard value or that the maximum average firing rate of fast inhibitory interneurons is twice than that of the others (see Eq 3 ). This is still consistent with the findings of Wendling et al [ 34 ] suggesting that impaired dendritic inhibition alters excitation-inhibition balance giving rise to rhythmic discharge activity capturing the effect of Penicillin G potassium in cortical tissues inhibiting GABA receptors [ 58 ]. Nevertheless, the estimated parameters indicate that our animal model of epilepsy can be best explained by much lower dendritic inhibition and much higher perisomatic inhibition compared to the standard range of values reported.…”

Section: Discussionsupporting

confidence: 92%

Differential temperature sensitivity of synaptic and firing processes in a neural mass model of epileptic discharges explains heterogeneous response of experimental epilepsy to focal brain cooling

et al. 2017

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Experiments with drug-induced epilepsy in rat brains and epileptic human brain region reveal that focal cooling can suppress epileptic discharges without affecting the brain’s normal neurological function. Findings suggest a viable treatment for intractable epilepsy cases via an implantable cooling device. However, precise mechanisms by which cooling suppresses epileptic discharges are still not clearly understood. Cooling experiments in vitro presented evidence of reduction in neurotransmitter release from presynaptic terminals and loss of dendritic spines at post-synaptic terminals offering a possible synaptic mechanism. We show that termination of epileptic discharges is possible by introducing a homogeneous temperature factor in a neural mass model which attenuates the post-synaptic impulse responses of the neuronal populations. This result however may be expected since such attenuation leads to reduced post-synaptic potential and when the effect on inhibitory interneurons is less than on excitatory interneurons, frequency of firing of pyramidal cells is consequently reduced. While this is observed in cooling experiments in vitro, experiments in vivo exhibit persistent discharges during cooling but suppressed in magnitude. This leads us to conjecture that reduction in the frequency of discharges may be compensated through intrinsic excitability mechanisms. Such compensatory mechanism is modelled using a reciprocal temperature factor in the firing response function in the neural mass model. We demonstrate that the complete model can reproduce attenuation of both magnitude and frequency of epileptic discharges during cooling. The compensatory mechanism suggests that cooling lowers the average and the variance of the distribution of threshold potential of firing across the population. Bifurcation study with respect to the temperature parameters of the model reveals how heterogeneous response of epileptic discharges to cooling (termination or suppression only) is exhibited. Possibility of differential temperature effects on post-synaptic potential generation of different populations is also explored.

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“…Figure b shows a representative real‐time signal recorded by a micropillar electrode, Ch‐9 , and Figure c is the normalized time‐frequency spectral analysis of the time‐series data. As shown in Figure d, three periods, including basal period, latent period, and epileptiform activity period, could be clearly identified, consistent with former study . The epileptiform activity period began with increasing discharges arising from the hyperexcitability and hypersynchrony of neuronal activity.…”

Section: Resultssupporting

confidence: 85%

Flexible Micropillar Electrode Arrays for In Vivo Neural Activity Recordings

Guan

Gao

et al. 2019

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Flexible electronics that can form tight interfaces with neural tissues hold great promise for improving the diagnosis and treatment of neurological disorders and advancing brain/machine interfaces. Here, the facile fabrication of a novel flexible micropillar electrode array (µPEA) is described based on a biotemplate method. The flexible and compliant µPEA can readily integrate with the soft surface of a rat cerebral cortex. Moreover, the recording sites of the µPEA consist of protruding micropillars with nanoscale surface roughness that ensure tight interfacing and efficient electrical coupling with the nervous system. As a result, the flexible µPEA allows for in vivo multichannel recordings of epileptiform activity with a high signal‐to‐noise ratio of 252 ± 35. The ease of preparation, high flexibility, and biocompatibility make the µPEA an attractive tool for in vivo spatiotemporal mapping of neural activity.

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Detailed spectral profile analysis of penicillin-induced epileptiform activity in anesthetized rats

Cited by 18 publications

References 23 publications

Suppressive Effects of Cooling Compounds Icilin on Penicillin G-Induced Epileptiform Discharges in Anesthetized Rats

Suppressive Effects of Cooling Compounds Icilin on Penicillin G-Induced Epileptiform Discharges in Anesthetized Rats

Differential temperature sensitivity of synaptic and firing processes in a neural mass model of epileptic discharges explains heterogeneous response of experimental epilepsy to focal brain cooling

Flexible Micropillar Electrode Arrays for In Vivo Neural Activity Recordings

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