Figure 1. Electrographic criteria of natural sleep states in the cat. 1–3, Contiguous epochs. The four ink-written traces represent the electrical activity of the thalamic LG visual nucleus, ocular movements (EOG), EEG waves from the surface of the association cortex and the activity of neck muscles (EMG). The arrow in 1 indicates transition from resting sleep to the pre-REM epoch, beginning with the first PGO wave. The first arrow in 2 points to EEG activation, while the second arrow indicates complete muscular atonia during REM sleep.

Figure 2. Activation of neocortical electrical activity produced by stimulation of mesopontine cholinergic nuclei in the cat. Top, slow oscillation and its disruption by a pulse-train (300 Hz, horizontal bar) to the pedunculopontine tegmental nucleus. The disruption of sleep slow waves upon arousal was associated with the appearance of fast activity, whose amplitude exceeded that of fast waves during sleep patterns. Numbers of recorded cortical foci correspond to those indicated on the association cortex (areas 5 and 7) of the brain diagram. Bottom, autocorrelations (AUTO, leads 1 to 5) and cross-correlations (CROSS, between leads 1–2 and 1–3) from sleep and aroused epochs (arrows). Note synchronized slow oscillation (0.5 Hz) during the sleep period and synchronization of fast rhythms (about 40 Hz) during the activated period. (Ecto., ectosylvian gyrus; marg., marginal gyrus.)

Figure 3. Thalamic generation of sleep spindles. (a) Circuit between thalamic reticular (RE), thalamocortical (Th-Cx) and cortical (Cx) neurons. The direction of axons is indicated by arrows. (b) Cellular bases of spindles. Intracellular recordings from RE, Th-Cx and Cx neurons in the cat. One spindle sequence is illustrated. In the RE neuron, the spindle consists of spike-bursts superimposed on a slowly growing and decaying depolarization. In the Th-Cx neuron, the spindle consists of rhythmic inhibitory postsynaptic potentials (IPSPs) that occasionally give rise to postinhibitory rebound spike-bursts. In the Cx neuron, the spike-bursts of the Th-Cx neuron trigger excitatory postsynaptic potentials (EPSPs) and action potentials within the frequency range of spindles.

Figure 4. The slow sleep oscillation. Dual simultaneous intracellular recordings from two cell-couples (a and b) in the right and left motor area 4 of cats. The EEGs from the depth of the same areas were also recorded. Note how the full synchronization of the EEG (starting at approximately the middle of depicted periods) was concomitant with simultaneous hyperpolarizations (downward deflections) in the two recorded neurons, in both (a) and (b). Also note spindles following the depth-negative (depolarizing) component of slow oscillation.

Figure 5. Inhibition of synaptic transmission in the thalamus, from the very onset of sleep. (a) Electrographic correlates of behavioural states of waking (W) and sleeping (S) states, with the transitional WS period of drowsiness. Normalized amplitudes (ordinates) of simultaneously recorded focal EEG cortical spindle waves (CSP trace) and delta waves (CS trace). Abscissa indicates real time. Note rhythmic sequences of spindle waves (oblique arrows) beginning with drowsiness (WS) and increased amplitudes of both spindles and delta waves during S. (b) Fluctuations in the amplitude of centrally evoked field potentials during W, drowsiness and S. Field potentials (superimposed traces) were recorded from the thalamic ventrolateral nucleus and were evoked by stimulation of afferent axons arising in the cerebellum. Note progressively diminished amplitude of monosynaptically relayed (r) wave during drowsiness, up to complete disappearance during sleep, in spite of lack of changes in the amplitude of the afferent (presynaptic) volley monitored by the tract (t) component.