On the activity of the corticostriatal networks during spike-and-wave discharges in a genetic model of absence epilepsy.

Absence seizures are characterized by impairment of consciousness associated with widespread bilaterally synchronous spike-and-wave discharges (SWDs) in the electroencephalogram (EEG), which reflect highly synchronized oscillations in thalamocortical networks. Although recent pharmacological studies suggest that the basal ganglia could provide a remote control system for absence seizures, the mechanisms of propagation of epileptic discharges in these subcortical nuclei remain unknown. In the present study, we provide the first description of the electrical events in the corticostriatal pathway during spontaneous SWDs in the genetic absence epilepsy rats from Strasbourg (GAERS), a genetic model of absence epilepsy. In corticostriatal neurons, the SWDs were associated with suprathreshold rhythmic depolarizations in-phase with local EEG spikes. Consistent with this synchronized firing in their excitatory cortical afferents, striatal output neurons (SONs) exhibited, during SWDs, large-amplitude rhythmic synaptic depolarizations. However, SONs did not discharge during SWDs. Instead, the rhythmic synaptic excitation of SONs was shunted by a Cl(-)-dependent increase in membrane conductance that was temporally correlated with bursts of action potentials in striatal GABAergic interneurons. The reduced SON excitability accompanying absence seizures may participate in the control of SWDs by affecting the flow of cortical information within the basal ganglia circuits.

Functional organization of the circuits connecting the cerebral cortex and the basal ganglia: implications for the role of the basal ganglia in epilepsy.

The basal ganglia are composed of a set of forebrain structures implicated in the adaptive control of behaviour. These structures process information originating from the entire cerebral cortex, as well as from nonspecific thalamic nuclei and the amygdala. In turn, they redistribute the integrated signals toward thalamic and brainstem nuclei related to motor, premotor, prefrontal and limbic cortical areas. During the two last decades, there has been increasing experimental evidence that the basal ganglia circuitry may be part of a remote control system influencing the spread of epileptic seizures. In the present article, we review the basic principles of the functional organization of the basal ganglia and provide experimental data on the activity that is transmitted by the cerebral cortex to the input stage of the basal ganglia during absence seizures. The functional organization of the basal ganglia supports the current hypothesis that these structures can dynamically control generalized seizures through their input-output relationships.