1. Multisite, extra- and intracellular recordings were carried out in cars under ketamine and xylazine anesthesia to assess the degree of synchrony and time relations among cellular activities in various neocortical fields during a slow (<1 Hz) oscillation consisting of long-lasting depolarizing and hyperpolarizing phases. 2. Recordings were performed from visual areas 17, 18, 19, and 21, association suprasylvian areas 5 and 7, motor pericruciate areas 4 and 6, as well as some related thalamic territories, such as the lateral geniculate (LG), perigeniculate (PG), and rostral intralaminal nuclei. We used spike analyses (auto- and cross-correlograms) to reveal rhythmicities, time relations and coherence properties, analyses of field potentials recorded through the same microelectrodes as used for unit discharges (auto-and cross-correlation functions and their spectral equivalents), and spike-triggered averages. The results are based on 194 groups of neurons with a total of 591 neurons. Seventeen groups included intracellular recordings of cortical neurons with membrane potentials more negative than -60 mV and overshooting action potentials. 3. The most obvious and frequent signs of neuronal synchrony were found within and between association areas 5 and 7 and 18/19 and 21. Closely located cells or neuronal pools were also ''closer'' in time. The shortest mean time lag was found between cells within adjacent foci (1-2 mm) of lag ras 5 and 7 and was 12 = 11.2 (SE) ms. with more caudal neurons preceding the rostral ones in 70% of cases. In visual cortical fields, the time lag between areas 18/19 and 21 neurons was 27.6 +/- 36 ms, between areas 17 and 21 was 36.2 +/- 47.8 ms. and between areas 18/19 and 17 was 40 +/- 73 ms. In the majority of cases, neuronal firing in area 21 preceded that in areas 18/19. The longest time lags were found in distant recordings from visual and motor areas, with a mean of 124 +/- 86.8 ms. although in some cell groups the time intervals between neuronal firing in areas 18/19 or 21 and areas 4 or 6 were as short as similar to 20 ms. 4. Similar time relations were found in those instances in which the unit Firing of the same cortical neuron was used as reference in spike triggered averages and was related to the field potential recorded from an adjacent area before impaling a neuron and, thereafter, to membrane potential fluctuations after impaling the cell. 5. The PG reticular thalamic neurons reflected the slow cortical oscillation in 75% of multisite recordings. The coherence between the slow rhythm of visual cortical cells and LG thalamocortical neurons was observed in 58% of cases. One-third of LG neurons displayed the intrinsically generated, clocklike delta oscillation that occurred synchronously in simultaneously recorded LG cells. 6. We discuss several possible scenarios implicated in the genesis of the slow cortical oscillation. Although relatively short time lags may be ascribed to direct and oligo- or multisynaptic connections between adjacent or distantly located cortical areas, long time laces (>50 ms) presumably involve inhibition-rebound sequences within the cortex or corticothalamocortical loops. In view of recent data indicating that the blockage of the slow oscillation during activated states could be achieved through a selective suppression of long-lasting inhibitory phases, we suggest that the major factors underlying short- or long-range neuronal synchrony during the slow oscillation are prolonged hyperpolarizations in cortical neuronal assemblies.
