Cortical slow oscillatory activity is reflected in the membrane potential and spike trains of striatal neurons in rats with chronic nigrostriatal lesions

Neurons in the basal ganglia output nuclei display rhythmic burst firing af ter chronic nigrostriatal lesions. The thalamocortical network is a strong endogenous generator of oscillatory activity, and the striatum receives a m assive projection from the cerebral cortex. Actually, the membrane potentia l of striatal projection neurons displays periodic shifts between a very ne gative resting potential (down state) and depolarizing plateaus (up states) during which they can fire action potentials. We hypothesized that an incr eased excitability of striatal neurons may allow transmission of cortical s low rhythms through the striatum to the remaining basal ganglia in experime ntal parkinsonism. In vivo intracellular recordings revealed that striatal projection neurons from rats with chronic nigrostriatal lesions had a more depolarized membrane potential during both the down and up states and an in creased firing probability during the up events. Furthermore, lesioned rats had significantly fewer silent neurons than control rats. Simultaneous rec ordings of the frontal electrocorticogram and membrane potential of striata l projection neurons revealed that the signals were oscillating synchronous ly in the frequency range 0.4-2 Hz, both in control rats and rats with chro nic nigrostriatal lesions. Spreading of the slow cortical rhythm is limited by the very low firing probability of control rat neurons, but a slow osci llation is well reflected in spike trains of similar to 60% of lesioned rat neurons. These findings provide in vivo evidence for a role of dopamine in controlling the flow of cortical activity through the striatum and may be of outstanding relevance for understanding the pathophysiology of Parkinson 's disease.