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Results: 7

1.
Figure 2

Figure 2. From: An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.

A. Phase contrast photo (4X) of an OHSC at DIV 21 - Cell layers of the dentate gyrus (DG), CA3 and CA1 are clearly visible. B. Field potential recording of OHSC- To test viability of OHSCs during field potential recording, the stimulating electrode is placed in the DG while the recording electrode is placed over the CA3 cell region. The trace shows an example of an evoked field potential recording from a viable OHSC. The stimulus artifact is followed by the field potential.

Julie M. Ziobro, et al. Brain Res. ;1371:110-120.
2.
Figure 6

Figure 6. From: An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.

Degree of cell death does not determine seizure activity - After glutamate injury, OHSCs displayed slightly varying degrees of cell death. However, the degree of cell death observed does not appear to play a role in the development of seizure activity. OHSCs were evaluated for cell death at 24 and 72 hours after glutamate injury on DIV 21. They were returned to the incubator until field potential recording at DIV 30-33. OHSCs that did not display seizure activity (white bars, n=39) did not significantly differ in PI uptake from OHSCs displaying seizures (gray bars, n=34).

Julie M. Ziobro, et al. Brain Res. ;1371:110-120.
3.
Figure 3

Figure 3. From: An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.

Extracellular recordings - Representative extracellular field potential recordings of CA3 cell layer of OHSCs at DIV 30. A. Control - Control OHSCs do not display seizure activity in aCSF. B. Glutamate treated - Representative field potential recording from an OHSC that was subjected to glutamate injury at DIV 21. Seizure activity is characterized by repetitive bursts of activity that last for longer than 3 seconds, changes over time and terminates. All vertical bars = 0.5mV

Julie M. Ziobro, et al. Brain Res. ;1371:110-120.
4.
Figure 4

Figure 4. From: An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.

Intracellular recording - Representative intracellular whole cell current clamp recordings of CA3 pyramidal cells at DIV 30. A. Control - Cells from control slices did not display repetitive bursting (n=9) B. Glutmate treated - Cells from glutamate treated slices displayed spontaneous recurrent epileptiform discharges (SREDs), similar to activity seen in extracellular field potential recordings. SREDs were observed in 43% of slice cultures following glutamate injury at DIV 21 (n=16).

Julie M. Ziobro, et al. Brain Res. ;1371:110-120.
5.
Figure 7

Figure 7. From: An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.

Standard AEDs are effective at blocking seizure activity - Representative field potential recordings of the effect of standard anti-epileptic drugs on seizure activity in glutamate treated slices at DIV 30. A. Phenytoin (200μM) is effective at blocking seizure activity during a 20 minute perfusion and can be washed out. On average, phenytoin decreased field potential amplitude by 23.4 ± 9.3 % (P=0.045) and frequency by 83.8 ± 4.6% (p<0.001, n=4) B. Phenobarbital (400μM) is also effective at blocking seizure activity during the 20 minute period of perfusion, amplitude decreased by 23.3 ± 8.5% (p=0.035) and frequency decreased by 77.3 ± 12.7% (p<0.001) following 15 minutes of drug perfusion (n=4). C. Ethosuximide (1 mM), is not effective at blocking seizure activity in glutamate injured OHSCs (p>0.05, n=4). All vertical bars = 0.1mV

Julie M. Ziobro, et al. Brain Res. ;1371:110-120.
6.
Figure 5

Figure 5. From: An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.

Development of seizures after injury - After glutamate injury (solid line), a significant percentage of OHSCs display seizure activity in field potential recordings as compared to age matched controls (dashed line). This change is long lasting and was observed up to 40 days in vitro. Within hours of injury (DIV 21), OHSCs did not display seizure events in either the control or injured groups (n=6 each). Between 3 and 8 days after injury (DIV 24-29), 40% of injured OHSCs and 0% of controls displayed seizure events (n=10 each, *p<0.05, Fisher’s exact test). In our established experimental time frame, DIV 30-33, we observed seizure events in 46.25% of glutamate injured OHSCs and 7.14% of controls (n=80, 28, **p<0.001, Chi-square analysis). By DIV 34-40, seizure events were observed in 50% of injured slices and 12.5% of controls (n=8, 9).

Julie M. Ziobro, et al. Brain Res. ;1371:110-120.
7.
Figure 1

Figure 1. From: An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.

A. Propidium Iodide uptake - Propidium Iodide (PI) uptake in OHSCs following 35 minute treatment with 3.5mM glutamate. PI staining indicates increased cell death in glutamate treated slices as compared to controls at both 24 and 72 hours following treatment. Note that significant cell death is observed in the CA1 cell region. (4X magnification). B. Comparison of PI uptake - Quantification of PI uptake in OHSCs at 24 and 72 hours after injury, expressed as a percent change from control. PI uptake was measured as mean optical density of the whole slice and normalized to age-matched controls. PI staining indicated a significant increase in cell death at both 24 (n=121, 174 for control and glutamate treated, respectively) and 72 hours (n=108, 154 for control and glutamate treated, respectively) after glutamate treatment (*p<0.001, Mann-Whitney Rank Sum test). C. PI uptake by cell region - At 24 hours, cell death is significantly higher in the CA1 cell region than it is in the dentate gyrus (DG) (*p<0.05, Kruskall-Wallis One Way ANOVA On Ranks). The CA3 region did not have a significant difference in PI uptake from either the CA1 or DG. At 72 hours, there is no significant difference in PI uptake between cell regions. (n=154)

Julie M. Ziobro, et al. Brain Res. ;1371:110-120.

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