An in vivo preparation has been developed to study the mechanisms underlyin
g spontaneous sleep oscillations. Dual and triple simultaneous intracellula
r recordings were made from neurons in small isolated cortical slabs (10 mm
x 6 mm) in anesthetized cats. Spontaneously occurring slow sleep oscillati
ons, present in the adjacent intact cortex, were absent in small stabs. How
ever, the isolated slabs displayed brief active periods separated by long p
eriods of silence, up to 60 s in duration. During these silent periods, 60%
of neurons showed non linear amplification of low-amplitude depolarizing a
ctivity. Nearly 40% of the cells, twice as many as in intact cortex, were c
lassified as intrinsically bursting. In cortical network models based on Ho
dgkin-Huxley-like neurons, the summation of simulated spontaneous miniature
excitatory postsynaptic potentials was sufficient to activate a persistent
sodium current, initiating action potentials in single neurons that then s
pread through the network. Consistent with this model, enlarging the isolat
ed cortical territory to an isolated gyrus (30 mm x 20 mm) increased the pr
obability of initiating large-scale activity. In these larger territories,
both the frequency and regularity of the slow oscillation approached that g
enerated in intact cortex. The frequency of active periods in an analytical
model of the cortical network accurately predicted the scaling observed in
simulations and from recordings in cortical slabs of increasing size.