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  • Title: Differential GABA(A) subunit expression following status epilepticus in seizure-prone and seizure-resistant rats: a putative mechanism for refractory drug response.
    Author: Gilby KL, Da Silva AG, McIntyre DC.
    Journal: Epilepsia; 2005; 46 Suppl 5():3-9. PubMed ID: 15987246.
    Abstract:
    PURPOSE: Two rat strains were selectively bred to be prone (Fast) or resistant (Slow) to amygdala kindling. The first objective of this experiment was to determine whether that selection was specific to kindling or was sensitive more broadly to another seizure induction agent, kainic acid (KA). Second, we investigated whether these strains exhibit distinct molecular responses to KA with respect to GABA(A) receptor subunit expression. METHODS: Development of status epilepticus (SE) was profiled in Fast and Slow rats injected with 20 mg/kg KA (i.p.). Two hours post-SE onset, rats received a sedative dose of sodium pentobarbital. Behavioral profiles included latency to SE, number of wet dog shakes (WDS), and number and duration of stage 3-5 generalized seizures. Rats were killed 24 h post-SE, and alpha(1) and alpha(4) mRNA levels were compared in the hippocampus and amygdala using QPCR. RESULTS: Slow rats exhibited a much greater latency to SE onset (p < 0.01) and many more WDS (p < 0.01) than Fast rats. During SE, Fast rats spent more time in and exhibited more repeated bouts of generalized stage 3-5 seizures (p < 0.01) than Slow rats. Constitutive levels of alpha1 and alpha4 were not different between the strains in either structure and equivalent reductions in alpha4 were evident 24 h post-SE. However, while Fast rats showed KA-induced reductions in alpha1 in both structures, Slow rats showed significant elevations. CONCLUSIONS: Genetic selection for temporal lobe excitability, manifested as differential amygdala kindling rates, is paralleled by vulnerability to KA-induced SE. Further, these strains exhibited at least one opposing molecular response to SE, namely alpha1 expression. This finding may offer a putative mechanism through which seemingly similar epilepsies can be intractable in some patients but treatable in others.
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