title: Discharge profiles across the sleep-waking cycle of identified cholinergic, GABAergic, and glutamatergic neurons in the pontomesencephalic tegmentum of the rat.
abstract: Distributed within the laterodorsal tegmental and pedunculopontine tegmental nuclei (LDT and PPT), cholinergic neurons in the pontomesencephalic tegmentum have long been thought to play a critical role in stimulating cortical activation during waking (W) and paradoxical sleep (PS, also called REM sleep), yet also in promoting PS with muscle atonia. However, the discharge profile and thus precise roles of the cholinergic neurons have remained uncertain because they lie intermingled with GABAergic and glutamatergic neurons, which might also assume these roles. By applying juxtacellular recording and labeling in naturally sleeping-waking, head-fixed rats, we investigated the discharge profiles of histochemically identified cholinergic, GABAergic, and glutamatergic neurons in the LDT, SubLDT, and adjoining medial part of the PPT (MPPT) in relation to sleep-wake states, cortical activity, and muscle tone. We found that all cholinergic neurons were maximally active during W and PS in positive correlation with fast (γ) cortical activity, as "W/PS-max active neurons." Like cholinergic neurons, many GABAergic and glutamatergic neurons were also "W/PS-max active." Other GABAergic and glutamatergic neurons were "PS-max active," being minimally active during W and maximally active during PS in negative correlation with muscle tone. Conversely, some glutamatergic neurons were "W-max active," being maximally active during W and minimally active during PS in positive correlation with muscle tone. Through different discharge profiles, the cholinergic, GABAergic, and glutamatergic neurons of the LDT, SubLDT, and MPPT thus appear to play distinct roles in promoting W and PS with cortical activation, PS with muscle atonia, or W with muscle tone.
authors.affiliation: Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada, and National Institute on Drug Abuse, Neuronal Networks Section, National Institutes of Health, Baltimore, Maryland 21224.
authors.forename: Soufiane
authors.initials: S
authors.lastname: Boucetta
authors.forename: Youssouf
authors.initials: Y
authors.lastname: Cissé
authors.forename: Lynda
authors.initials: L
authors.lastname: Mainville
authors.forename: Marisela
authors.initials: M
authors.lastname: Morales
authors.forename: Barbara E
authors.initials: BE
authors.lastname: Jones
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001710:Biotin / Q000031:analogs & derivatives / Q000378:metabolism; D002452:Cell Count; D002940:Circadian Rhythm; D004569:Electroencephalography; D004576:Electromyography; D005968:Glutamate Decarboxylase / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000145:classification / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D020318:Rats, Long-Evans; D012890:Sleep / Q000502:physiology*; D013681:Tegmentum Mesencephali / Q000166:cytology* / Q000502:physiology; D050494:Vesicular Acetylcholine Transport Proteins / Q000378:metabolism; D050599:Vesicular Glutamate Transport Protein 2 / Q000378:metabolism; D014851:Wakefulness / Q000502:physiology*
chemical_list: D050494:Vesicular Acetylcholine Transport Proteins; D050599:Vesicular Glutamate Transport Protein 2; C070614:neurobiotin; D001710:Biotin; D005968:Glutamate Decarboxylase
keywords: EEG; EMG; REM sleep; paradoxical sleep; slow-wave sleep