Discharge patterns of cat pontine brain stem neurons during desynchronized sleep

1. Discharge pattern has been characterized by autocorrelation analysis of stationary portions of extracellularly recorded discharge trains of cat pontine brain stem neurons during spontaneously occurring desynchronized sleep episodes. 2. Neurons localized to the area implicated in control of the desynchronized phase of sleep, the gigantocellular tegmental field (FTG), show the most phasic or clustered discharge pattern, as evinced by initial peaks in the autocorrelations. At the peak, the FTG population average discharge probability is 3 times that expected had the discharges been evenly distributed over time. The initial peak extends beyond a lag of 3 s, indicating runs of clustered discharge extending beyond this duration. Neurons in other reticular tegmental fields, the tegmental reticular nucleus and pontine gray, show a more sustained or tonic discharge pattern. 3. Discharge patterns of a given cell are consistent from one desynchronized sleep episode to the next; units with phasic discharge patterns remain phasic, and tonic patterns remain tonic. 4. There is a three-way correlation among FTG units recorded at sites with many giant cells, units with high discharge rate increases on transition to desynchronized sleep, and units with a markedly phasic discharge pattern. This implicates the giant cells as the source of both the distinctive discharge rate and pattern changes of neurons during desynchronized sleep. 5. Stereotyped, regular discharge patterns are not characteristic of FTG or other units, suggesting they are not pacemakers and that endogenous activation of pacemaker cells is unlikely to be a mechanism for generation of the marked discharge rate increases on transition to desynchronized sleep that are found in FTG units. The irregular, clustered discharge pattern of FTG is more compatible with generation of discharge rate increases through interaction with other cells. The markedly phasic discharge of FTG units is also consistent with a driving role in generation of the phasic electrophysiologic events of desynchronized sleep.