Abstract
Albino rats have a higher amplitude of the late complex of the flash-induced visual evoked potential (VEPs) and afterdischarges (AD), the latter in particular during low states of arousal and vigilance than hooded and pigmented rats. These ADs are generated in cortico-geniculate-cortical pathways and have been used as a model for the evaluation of putative anti-absence drugs, while properties of flash-evoked VEPs were also used to predict toxic effects of new compounds, including putative anticonvulsant drugs. Flash VEPs made during spike-wave discharges (SWDs) in the genetic animal absence models have revealed that their sensory system is largely intact; interestingly the state of the brain during SWDs mimics that of slow-wave sleep. Photic stimulation in the genetic epileptic models does not provoke a photoparoxysmal response, as has been found in some absence epilepsy patients. However, trains of intense photic stimulation was efficacious in inducing neuroplastic changes leading to photoparoxysmal activity in normal young adult Sprague-Dawley rats. SWDs originating from the somatosensory cortex in the genetic rat models were reduced during photic stimulation due to enhanced arousal. Moreover, outcomes from fMRI studies in absence patients showed that the pathways and the brain regions involved in the occurrence of spontaneous occurring SWDs differ from those involved in the SWDs elicited by photic stimulation. Although both SWDs and flash-evoked AD are cortico-thalamo-cortical oscillations, it seems that there are important differences between the rodent absence models, regarding the brain networks and mechanisms and humans with absence seizures between physiological elicited photically induced ADs and the spontaneous occurring pathological SWDs.
