Mechanisms of long‐lasting hyperpolarizations underlying slow sleep oscillations in cat corticothalamic networks.

Abstract

1. To explore the nature of the long‐lasting hyperpolarizations that characterize slow oscillations in corticothalamic circuits in vivo, intracellular recordings were obtained under ketamine‐xylazine anaesthesia from cortical (Cx) cells of the cat precruciate motor cortex, thalamic reticular (RE) cells from the rostrolateral sector, and thalamocortical (TC) cells from the ventrolateral (VL) nucleus. 2. Measurements in the three cell types showed input resistance (Rin) to be highest during the long‐lasting hyperpolarizations that correspond to depth‐positive waves of the cortical EEG. Rin was lowest during the early phase of high‐amplitude depth‐negative EEG waves and increased thereafter until the next cycle of the slow oscillation. 3. Spontaneous long‐lasting hyperpolarizations were compared with those evoked by dorsal thalamic stimulation. Voltage versus current (V‐I) plots showed similar membrane potential (Vm) ranges and slopes for spontaneous and evoked hyperpolarizations in both Cx and RE cells. V‐I plots from TC cells had similar slopes, but Vm during evoked hyperpolarizations was displaced towards more negative values. 4. Intracellular injection of constant hyperpolarizing current in Cx cells increased the amplitude of the initial part of the depolarizing plateau of the slow oscillation, but decreased the amplitude of the last part. 5. These results suggest disfacilitation to be the dominant mechanism in the membrane of cortical and thalamic cells during the spontaneous long‐lasting hyperpolarizations, which shape and synchronize slow oscillations in corticothalamic networks. In Cx and RE cells, the same mechanism underlies thalamically evoked long‐lasting hyperpolarizations. By contrast, evoked responses in TC cells show a strong additional hyperpolarizing factor. We propose that GABAB processes are stronger in TC than in Cx neurones, thus rendering the thalamus an easier target for absence‐type epileptic phenomena through potentiation of thalamic rebound capabilities.