Bulbo-thalamic neurons related to thalamocortical activation processes during paradoxical sleep

Abstract

Neurons histologically localized in the gigantocellular (Gc) and magnocellular (Mc) fields of the bulbar reticular formation were tested for antidromic invasion by stimulating the ventromedial (VM) and intralaminar (centralis lateralis, CL, and centrum medianum, CM) thalamic nuclei, midbrain reticular formation (MRF), and reticulospinal tract. An overwhelming majority (94%) of antidromically identified cells projected either to rostral structures (MRF, medial and intralaminar thalamic nuclei) or to the spinal cord, while only 6% had bifurcating axons. Rostrally projecting bulbar reticular neurons were investigated during various wake-sleep behavioral states. (a) Phasic neurons were related to PGO waves, eye and head movements, and were localized in both Gc and Mc fields. (b) The majority of tonic neurons projected to MRF and VM and they were localized within Mc in a proportion of 85%. In order to test their possible role in activation of thalamocortical processes (as betrayed by EEG desynchronization), the activity of tonically discharging cells was separately evaluated in periods with and without phasic motor events. Half of the tonically discharging neurons had a high selectivity of discharge during paradoxical sleep without REM bursts (PS-); the ratio of their mean discharge rate during PS- to that in quiet wakefulness ( QW ) or slow-wave sleep (SWS) was 8 and 6, respectively. The other half of the tonic neurons equally increased firing rates from SWS to either QW or PS. The firing rate of rostrally projecting bulbar reticular neurons with tonic discharge patterns was analyzed during transitions from SWS to PS. An increase in discharge rate was found about 30 to 60 s prior to the first sign of EEG desynchronization in PS, during fully synchronized sleep with PGO waves (S-PGO). Statistical testing showed that the increased firing rate was not associated to PGO waves, but was temporally related to the appearance of EEG desynchronization at PS onset. We conclude, on the basis of these and other recent data, that tonically discharging bulbar reticular neurons with identified projections to the midbrain and thalamic nuclei act synergically with rostrally projecting MRF neurons as sources of thalamocortical activation.