Voltage-dependent 40-Hz oscillations in rat reticular thalamic neurons in vivo.

Extra- and intracellular recordings of thalamic reticular and relay neurons were performed in rats under urethane anaesthesia. Under this type of anaesthesia it was found that, throughout the whole reticular thalamic nucleus, a large proportion of cells (approximately 34%) discharged like clocks within a 25-60 Hz frequency band width (i.e. 40 Hz). Simultaneous recordings of pairs of reticular cells showed that the regular discharges of nearby units were not synchronous. Thus, the asynchronous 40-Hz firing of reticular thalamic cells was not correlated with any 40-Hz extracellular activity as revealed by the spectral analysis of the electroencephalogram and by recordings performed in various thalamic nuclei. In relay cells of the ventrobasal, ventral lateral and posterior thalamic nuclei, the regular firing of reticular thalamic neurons induced a rhythmic inhibitory modulation that was detected by the time-series analysis of the inhibitory postsynaptic potentials. In many relay cells, however, the disclosure of this inhibitory modulation required cellular depolarization since the resting potential in these cells was maintained at the reversal potential of the inhibitory events. Intracellular recordings of reticular thalamic cells showed that their regular firing was not driven in an all-or-nothing manner by 40-Hz synaptic inputs but rather that it depended upon the activation of a voltage-dependent pacemaker mechanism; this pacemaker activity was manifested by the presence of subthreshold oscillations that drove spike discharges and whose frequency was voltage dependent. In the context of data already published on the genesis of 40-Hz oscillations in the brain, and given the key position of reticular thalamic neurons in thalamocortical networks, the present results indicate that the reticular thalamic nucleus might play a pacemaker function in the genesis of 40-Hz oscillations in the thalamus and cortex during states of focused arousal.