title: A5 cells are silenced when REM sleep-like signs are elicited by pontine carbachol.
abstract: The A5 noradrenergic neurons are considered important for cardiorespiratory regulation. We hypothesized that A5 cells are silenced during rapid eye movement (REM) sleep, thereby contributing to cardiorespiratory changes and suppression of hypoglossal (XII) motoneuronal activity. We used an anesthetized, paralyzed, and artificially ventilated rat in which pontine microinjections of carbachol trigger signs of REM sleep, including hippocampal theta rhythm, motor suppression, and silencing of locus coeruleus neurons. All 16 putative noradrenergic A5 cells recorded were strongly suppressed when the REM sleep-like episodes were elicited and also after intravenous clonidine. Antidromic mapping showed that none of six neurons tested projected to the XII nucleus, whereas three of five projected to the nucleus of the solitary tract and two of four to the rostral ventrolateral medulla. Bilateral microinjections of clonidine into the A5 regions did not alter XII nerve activity. These data suggest that A5 neurons are silenced during natural REM sleep. This will lead to decreased norepinephrine release and may alter synaptic transmission in the nucleus of the solitary tract and rostral ventrolateral medulla without, however, a detectable impact on XII motoneurons.
authors.affiliation: Department of Animal Biology, School of Veterinary Medicine, and Center for Sleep and Respiratory Neurobiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6046, USA. vfenik@vet.upenn.edu
authors.forename: Victor
authors.initials: V
authors.lastname: Fenik
authors.forename: Vitaliy
authors.initials: V
authors.lastname: Marchenko
authors.forename: Patrick
authors.initials: P
authors.lastname: Janssen
authors.forename: Richard O
authors.initials: RO
authors.lastname: Davies
authors.forename: Leszek
authors.initials: L
authors.lastname: Kubin
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D001369:Axons / Q000502:physiology; D002217:Carbachol / Q000008:administration & dosage / Q000494:pharmacology*; D018679:Cholinergic Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D003000:Clonidine / Q000008:administration & dosage / Q000494:pharmacology; D004569:Electroencephalography; D004594:Electrophysiology; D007002:Hypoglossal Nerve / Q000187:drug effects / Q000502:physiology; D007275:Injections, Intravenous; D008526:Medulla Oblongata / Q000502:physiology; D008845:Microinjections; D009433:Neural Inhibition / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D011149:Pons / Q000166:cytology / Q000187:drug effects* / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012895:Sleep, REM / Q000502:physiology*; D017552:Solitary Nucleus / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology
chemical_list: D000316:Adrenergic alpha-Agonists; D018679:Cholinergic Agonists; D002217:Carbachol; D003000:Clonidine