Wild-caught BN rats displayed absence-like SWD/immobility events that were highly similar to outbred BN rats in terms of spike-wave morphology, frequency, diurnal rhythmicity, associated immobility, and sensitivity to the anti-absence drug, ethosuximide however, SWD bursts were less frequent and of shorter duration in wild-caught and outbred BN rats than the outbred Long–Evans and inbred WAG/Rij strains. ![]() To test this hypothesis, we compared chronic video/electrocorticogram recordings from male and female wild-caught (Brown-Norway ) rats to recordings from laboratory outbred BN, outbred Long–Evans, and inbred WAG/Rij rats (i.e., a model of absence epilepsy). We hypothesized that, if SWD/immobility models absence seizures, it would not exist in wild-caught rats due to the pressures of natural selection. However, these events are also common in outbred laboratory rats, raising concerns about whether SWD/immobility accurately reflects absence epilepsy as opposed to “normal” rodent behavior. Genetic models of this disorder have been created by selectively inbreeding rats for absence seizure-like events with similar electrical and behavioral characteristics. ![]() Absence epilepsy is a heritable human neurological disorder characterized by brief nonconvulsive seizures with behavioral arrest, moderate-to-severe loss of consciousness (absence), and distinct spike-wave discharges (SWDs) in the EEG and electrocorticogram (ECoG).
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