Effects of Anticonvulsants on Penicillin‐Induced Bursting in Guinea Pig Hippocampal Slices

Schneiderman, Jacob; Evans, James

doi:10.1111/j.1528-1157.1986.tb03552.x

Cited by 16 publications

(4 citation statements)

References 26 publications

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“…The concentrations of diazepam and midazolam used in our experiments are also comparable with those in other in vitro slice models of epileptiform activity. When epileptiform activity was induced by penicillin in guinea pig hippocampal slices, diazepam (Ϸ10 M) was required to consistently block bursting (Schneiderman and Evans, 1986), whereas an IC 50 of Ϸ12 M was determined for midazolam to inhibit low Ca 2ϩ -induced bursting in the guinea pig hippocampal slice (Ashton et al, 1988). Overall, the data obtained with the benzodiazepines are in accord with the known in vivo pharmacology of OP-induced seizures and are comparable with other in vitro models of epileptiform activity.…”

Section: Discussionsupporting

confidence: 73%

A Guinea Pig Hippocampal Slice Model of Organophosphate-Induced Seizure Activity

Harrison¹,

Sheridan²,

Green³

et al. 2004

J Pharmacol Exp Ther

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Extracellular recording techniques have been used in the guinea pig hippocampal slice preparation to investigate the electrophysiological actions of the organophosphate (OP) anticholinesterase soman. When applied at a concentration of 100 nM, soman induced epileptiform activity in the CA1 region in approximately 75% of slices. This effect was mimicked by the anticholinesterases paraoxon (1 and 3 M), physostigmine (30 M), and neostigmine (30 M), thus providing indirect evidence that the epileptiform response was mediated by elevated acetylcholine levels. Soman-induced bursting was inhibited by the muscarinic receptor antagonists atropine (concentrations tested, 0

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Section: Discussionsupporting

confidence: 73%

A Guinea Pig Hippocampal Slice Model of Organophosphate-Induced Seizure Activity

Harrison¹,

Sheridan²,

Green³

et al. 2004

J Pharmacol Exp Ther

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“…A number of studies have shown that known anticonvulsants have inhibitory effects on epileptiform bursting in hippocampal slices bathed in media containing pentylenetetrazole (Piredda et al, 1986), penicillin (Schneiderman and Evans, 1986), and elevated potassium (Korn et al, 1987). However, a primary disadvantage of these models is their reliance on drug or ionic manipulations to generate epileptiform bursting.…”

mentioning

confidence: 99%

Differential Effects of Phenobarbital and Pentobarbital on Stimulus Train‐Induced Bursting in the Hippocampal Slice

Swartzwelder

Wilson

1987

Epilepsia

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Stimulus train-induced bursting (STIB) in the hippocampal slice is an in vitro model of epileptiform activity that is analogous to kindling and requires no manipulation of the neurochemical or ionic environment. The bursts recorded from slices after STIB closely resemble the discharges observed in vivo after kindling and may provide a convenient and accessible model for studies of the electrophysiological underpinnings of epileptiform bursting in local neural circuits. One critical element in the validation of this model is the responsiveness of STIB to traditional sedatives and anticonvulsants. In this study we assessed the effects of the barbiturates phenobarbital and pentobarbital on both spontaneous and stimulus-triggered bursts after STIB. Concentration-response studies indicated that both drugs had inhibitory effects on stimulus-triggered bursting, although at significantly different concentrations. The rate of spontaneous bursting, however, was not significantly affected by phenobarbital at any of the concentrations tested, whereas pentobarbital reduced the frequency of spontaneous bursting in a concentration-dependent manner. These results indicate that STIB is responsive to the barbiturates tested, although the drugs have differential potencies depending on the type of bursting measured. These effects may be the result of differential potencies of these drugs on gamma-aminobutyric acid-mediated inhibition within local hippocampal circuits, as well as different effects on the biophysical characteristics of pacemaker cells within these circuits.

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“…We analyzed changes in interburst interval, burst length, and CA3 burst synchronization. In general, DPH has been identified as a prototypic, sodium channel, anticonvulsant compound and has been used clinically for partial and generalized seizures (Griffith and Taylor, 1988a; Johannessen, 2002; Korn et al, 1987; Levine and Chang, 1990; Oliver et al, 1977; Schneiderman and Evans, 1986; Schneiderman and Schwartzkroin, 1982). RLZ has been shown to block the persistent sodium current (I NaP ; Cheah et al, 2010; Harvey et al, 2006; Miles et al, 2005; Theiss et al, 2007; Urbani and Belluzzi, 2000) whereas, LIDO has demonstrated the ability to inhibit voltage-gated sodium channels during abnormal membrane depolarization (Ragsdale et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Diphenytoin, riluzole and lidocaine: Three sodium channel blockers, with different mechanisms of action, decrease hippocampal epileptiform activity

et al. 2013

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Epilepsy is a condition affecting 1–2% of the population, characterized by the presence of spontaneous, recurrent seizures. The most common type of acquired epilepsy is temporal lobe epilepsy (TLE). Up to 30% of patients with TLE are refractory to currently available compounds, and there is an urgent need to identify novel targets for therapy. Here, we utilized the in-vitro CA3 burst preparation to examine alterations in network excitability, characterized by changes in interburst interval and bursting thresholds. Specifically, we show that bath application of three different sodium channel blockers—diphenytoin, riluzole, and lidocaine—slow spontaneous CA3 bursts. This in turn, decreased the epileptiform activity. These compounds work at different sites on voltage-gated sodium channels, but produce a similar network phenotype of decreased excitability. In the case of diphenytoin and riluzole, the change in network activity (i.e., increased interburst intervals) was persistent following drug washout. Lidocaine application, however, only increased the CA3 interburst interval when it was in the bath solution. Thus, its action was not permanent and resulted in returning CA3 bursting to baseline levels. These data demonstrate that the CA3 burst preparation provides a relatively easy and quick platform for identifying compounds that can decrease network excitability, providing the initial screen for further and more complex in-vivo, freely-behaving animal studies.

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Effects of Anticonvulsants on Penicillin‐Induced Bursting in Guinea Pig Hippocampal Slices

Cited by 16 publications

References 26 publications

A Guinea Pig Hippocampal Slice Model of Organophosphate-Induced Seizure Activity

A Guinea Pig Hippocampal Slice Model of Organophosphate-Induced Seizure Activity

Differential Effects of Phenobarbital and Pentobarbital on Stimulus Train‐Induced Bursting in the Hippocampal Slice

Diphenytoin, riluzole and lidocaine: Three sodium channel blockers, with different mechanisms of action, decrease hippocampal epileptiform activity

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