MECHANISMS OF LONG-LASTING HYPERPOLARIZATIONS UNDERLYING SLOW SLEEP OSCILLATIONS IN CAT CORTICOTHALAMIC NETWORKS

1. To explore the nature of the long-lasting hyperpolarizations that c haracterize slow oscillations in corticothalamic circuits in vivo, int racellular recordings were obtained under ketamine-xylazine anaesthesi a from cortical (Cx) cells of the cat precruciate motor cortex, thalam ic reticular (RE) cells from the rostrolateral sector, and thalamocort ical (TC) cells from the ventrolateral (VL) nucleus. 2. Measurements i n the three cell types showed input resistance (R(in)) to be highest d uring the long-lasting hyperpolarizations that correspond to depth-pos itive waves of the cortical EEG. R(in) was lowest during the early pha se of high-amplitude depth-negative EEG waves and increased thereafter until the next cycle of the slow oscillation. 3. Spontaneous long-las ting hyperpolarizations were compared with those evoked by dorsal thal amic stimulation. Voltage versus current (V-I) plots showed similar me mbrane potential (V-m) ranges and slopes for spontaneous and evoked hy perpolarizations in both Cx and RE cells. V-I plots from TC cells had similar slopes, but V-m during evoked hyperpolarizations was displaced towards more negative values. 4. Intracellular injection of constant hyperpolarizing current in Cx cells increased the amplitude of the ini tial part of the depolarizing plateau of the slow oscillation, but dec reased the amplitude of the last part. 5. These results suggest disfac ilitation 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 net works. In Cx and RE cells, the same mechanism underlies thalamically e voked long-lasting hyperpolarizations. By contrast, evoked responses i n TC cells show a strong additional hyperpolarizing factor. We propose that GABA(B), processes are stronger in TC than in Cx neurones, thus rendering the thalamus an easier target for absence-type epileptic phe nomena through potentiation of thalamic rebound capabilities.