Representative traces of effects of AEDs (PHT, VPA) and washout upon neuronal population spike events.

<p>Spike events over 1-minute intervals were from one continuous recording during baseline, drug applications and washout, for qualitative displays.</p

Example of epileptiform discharges observed in the stratum pyramidale of the high-K⁺ treated hippocampal slices.

<p>Example of epileptiform discharges observed in the stratum pyramidale of the high-K⁺ treated hippocampal slices.</p

Effects of PHT, VPA applied singly and in combination upon frequency of spike events.

<p>Data from combined recordings of CA1 and CA3 regions were expressed as relative percentage (%) reduction compared to the baseline. All data were shown as mean ± SEM; “n” indicates the number of recordings.</p

Effects of PHT, VPA applied in isolation and in combination upon frequency of spike events.

<p>Data were expressed as relative percentage (%) reduction compared to the baseline. All data were shown as mean ± SEM; “n” indicates the number of recordings from different slices. See text for details.</p

Representative traces of effects of AEDs (LTG, VPA) and washout upon neuronal population spike events.

<p>Representative 1-minute intervals of spike events during baseline, drug applications and washout from one continuous recording are displayed.</p

Effects of LTG, VPA applied in isolation and in combination upon frequency of spike events.

<p>Data were expressed as relative percentage (%) reduction compared to the baseline. All data were shown as mean ± SEM; “n” indicates the number of recordings from different slices. See text for details.</p

Dose responses of PHT and VPA in suppressing population spike events in the high-K⁺ model.

<p>Data from combined recordings of CA1 and CA3 regions were expressed as relative percentage (%) reduction compared to the baseline. (<b>A</b>) The effect of PHT on spike frequency was taken during the final 1-minute interval following 3-minute drug applications. (<b>B</b>) The effect of VPA on spike frequency was taken over the stable final 2-minute interval following 6-minute applications of VPA and washout. All data were shown as mean ± SEM; “n” indicates the number of recordings.</p

NPY mRNA expression is increased in the thalamus of valproate treated GAERS.

<p>Representative coronal pictures of dissected tissue from SCx (A); Thal (B); Arc (C). (D) NPY mRNA expression (relative to 18S mRNA expression) was significantly increased in the thalamus of valproate treated GAERS (black bars n = 6) compared to saline treated GAERS (white bars n = 6). Data shown as mean±SEM. *p<0.05 compared to saline controls (two tailed Mann Whitney U test). Thal - thalamus; SCx - Somatosensory cortex; Arc -arcuate nucleus.</p

Five days of valproate treatment suppresses seizures in GAERS.

<p>(A) Representative EEG trace from a GAERS rat showing the characteristic spike-and-wave discharge of an absence seizure. GAERS were given valproate (black bars n = 6; 42 mg.kg-1 hr-1) or saline (white bars n = 6) continuously for 5 days. 24 hour EEG data were collected and the percent of time spent in seizure activity (B), number of seizures per hour (C) and seizure duration (D) was quantified for each animal. A two-tailed Mann Whitney U test at each time point shows that the percentage of time spent in seizure activity (B) and the number of seizures per hour (C) was significantly reduced only after five days of treatment. Data shown as mean±SEM *p<0.05 valproate treatment compared to saline control.</p

Valproate does not affect food intake in GAERS.

<p>Food intake in saline (white bars n = 6) and valproate (black bars n = 6) treated GAERS at baseline and over the 5 day treatment period. There was no significant difference in food intake between GAERS receiving valproate compared to GAERS receiving saline treatment on each day of treatment (p>0.05, two-tailed Mann Whitney U test). Data shown as mean±SEM.</p