Epileptiform synchronization and high-frequency oscillations in brain slices comprising piriform and entorhinal cortices

Hamidi, Shabnam; Lévesque, Maxime

doi:10.1016/j.neuroscience.2014.09.065

Cited by 17 publications

(16 citation statements)

References 29 publications

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“…We have confirmed here that ionotropic glutamatergic receptor-mediated signaling is required for the generation of ictal discharges in both PC and EC (Avoli et al, 2013;Hamidi et al, 2014;Herrington et al, 2014). In keeping with evidence obtained in these previous studies, we have found that blockade of glutamatergic signaling using NMDA and non-NMDA receptor antagonists led to the occurrence of isolated, slow GABA receptordependent potentials during application of 4AP.…”

Section: Modulation Of Isolated Gabaergic Events By Kcc2 Blockers Andsupporting

confidence: 91%

“…To identify oscillations in each frequency range (80-200 Hz and 250-500 Hz), a multi-parametric algorithm was employed using routines based on standardized functions (Matlab Signal Processing Tool-box) as described in detail in Hamidi et al (2014) and Salami et al (2012).…”

Section: Methodsmentioning

confidence: 99%

“…Field potential recordings-which were obtained simultaneously from PC and EC during 4AP application-revealed ictal and interictal discharges that occurred in both structures (Hamidi et al, 2014) (Fig. 1B).…”

Section: Effects Of Kcc2 Blockers On 4ap-induced Epileptiform Activitymentioning

confidence: 99%

“…Finally, we pharmacologically blocked glutamatergic transmission with CPP (10 μM) and CNQX (10 μM) to analyze the effects of VU0240551, bumetanide (50 μM) and CLP257 on the 4AP-induced isolated GABAergic events that are recorded under these conditions (Hamidi et al, 2014). As shown in Figs.…”

Section: Kcc2 Blockers and Pharmacologically Isolated Synchronous Eventsmentioning

confidence: 99%

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KCC2 function modulates in vitro ictogenesis

Hamidi

Avoli

2015

Neurobiology of Disease

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GABA A receptor-mediated inhibition is active and may contribute to epileptiform synchronization. The efficacy of inhibition relies on low levels of intracellular Cl − , which are controlled by KCC2 activity. This evidence has led us to analyze with field potential recordings the effects induced by the KCC2 blockers VU0240551 (10 μM) or bumetanide (50 μM) and by the KCC2 enhancer CLP257 (100 μM) on the epileptiform discharges generated by piriform and entorhinal cortices (PC and EC, respectively) in an in vitro brain slice preparation. Ictal-and interictal-like discharges along with high-frequency oscillations (HFOs, ripples: 80-200 Hz, fast ripples: 250-500 Hz) were recorded from these two regions during application of 4-aminopyridine (4AP, 50 μM). Blocking KCC2 activity with either VU024055 or high doses of bumetanide abolished ictal discharge in both PC and EC; in addition, these experimental procedures decreased the interval of occurrence and duration of interictal discharges. In contrast, enhancing KCC2 activity with CLP257 increased ictal discharge duration in both regions. Finally, blocking KCC2 activity decreased the duration and amplitude of pharmacologically isolated synchronous GABAergic events whereas enhancing KCC2 activity led to an increase in their duration. Our data demonstrate that in vitro ictogenesis is abolished or facilitated by inhibiting or enhancing KCC2 activity, respectively. We propose that these effects may result from the reduction of GABA A receptor-dependent increases in extracellular K + that are known to rest on KCC2 function.

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Section: Modulation Of Isolated Gabaergic Events By Kcc2 Blockers Andsupporting

confidence: 91%

Section: Methodsmentioning

confidence: 99%

Section: Effects Of Kcc2 Blockers On 4ap-induced Epileptiform Activitymentioning

confidence: 99%

Section: Kcc2 Blockers and Pharmacologically Isolated Synchronous Eventsmentioning

confidence: 99%

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KCC2 function modulates in vitro ictogenesis

Hamidi

Avoli

2015

Neurobiology of Disease

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“…Our group has previously characterized 4AP-induced epileptiform discharges in PC and EC (Hamidi et al, 2014) and has reported the effects of neurosteroids on such epilepti-form activity and HFOs in the PC of healthy rats (Herrington et al, 2013). It remains however unknown whether these effects are maintained in the epileptic brain.…”

Section: Introductionmentioning

confidence: 99%

Neurosteroidal modulation of in vitro epileptiform activity is enhanced in pilocarpine-treated epileptic rats

Shiri

Herrington

Lévesque

2015

Neurobiology of Disease

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We employed field potential recordings in brain slices obtained from pilocarpine-treated epileptic (4-5 weeks following a pilocarpine-induced status epilepticus) and age-matched, non-epileptic control (NEC) rats to establish the effects of the neurosteroid allotetrahydrodeoxycorticosterone (THDOC) on the epileptiform activity -including high frequency oscillations (HFOs; ripples: 80-200 Hz, fast ripples: 250-500 Hz) -induced by 4-aminopyridine (4AP) in piriform (PC) and entorhinal (EC) cortices. Both structures are highly susceptible to generate seizures and may also be involved in epileptogenesis. We found that THDOC application to pilocarpine-treated slices: (i) decreased interictal discharge frequency in PC while increasing it in EC; (ii) abolished ictal discharges in both areas in approx. one third of the experiments and reduced them in frequency and duration in the remaining experiments; and (iii) increased the occurrence of ripples and fast ripples associated to interictal events, and modified their pattern of occurrence during ictal discharges in both PC and EC. These effects were either weaker or absent in NEC tissue. Our results demonstrate that THDOC plays a structure-dependent modulatory role in epileptiform synchronization in the pilocarpine-treated epileptic rat brain where its actions are more pronounced than in NEC tissue. This evidence supports the application of neurosteroids as potential antiepileptic tools.

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