Abstract
Tuberomamillary (TM) histamine (HA) neurons play an important role in the mechanisms of wakefulness (W). We have recently shown in the mouse that identified HA neurons are waking-specific and that they are all characterized by triphasic broad action potential. It is currently believed that HA neurons cease firing during sleep by an inhibitory mechanism mediated by GABAergic sleep-promoting neurons in the preoptic area (POA). In order to test this assumption, we have recorded single unit activity from the TM and POA in head-restrained, conscious mice and determined their unit activity profiles at the state transitions. Forty-two waking-specific neurons were recorded in the TM, while 7 slow-wave sleep (SWS)-specific and 8 SWS/paradoxical sleep (PS)-specific neurons were recorded in the POA. At the transition from W to SWS, TM HA neurons stopped firing clearly before the onset of EEG synchronization, the first sign of EEG sleep, with a mean (± S.E.M) latency of 1078.3 ± 72.7 ms, while both POA SWS-specific and SWS/PS-specific neurons began firing either at the onset or after the onset of EEG synchronization. At the transition from SWS to W, HA neurons displayed firing with a long delay (800.2 ± 62.7 ms) after the onset of EEG desynchronization, while the POA sleep-specific neurons stopped firing prior to the onset of EEG desynchronization. These results suggest that the neuronal activity of HA neurons during behavioral states is not controlled exclusively by POA sleep-promoting neurons. [J Physiol Sci. 2007;57 Suppl:S73]
