Heart rate variability during carbachol-induced REM sleep and cataplexy

• Published in: Behavioural brain research Vol. 291; pp. 72 - 79
• Main Authors: Torterolo, Pablo, Castro-Zaballa, Santiago, Cavelli, Matías, Velasquez, Noelia, Brando, Victoria, Falconi, Atilio, Chase, Michael H., Migliaro, Eduardo R.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15.09.2015
• Subjects: Animals; Autonomic system; Carbachol - pharmacology; Cardiovascular Agents - pharmacology; Cataplexy - chemically induced; Cataplexy - physiopathology; Cats; Cholinergic; Cholinergic Agonists - pharmacology; Electrocardiography; Heart Rate - drug effects; Heart Rate - physiology; HRV; Narcolepsy; Polysomnography; Pontine Tegmentum - drug effects; Pontine Tegmentum - physiopathology; Respiration - drug effects; Reticular formation; Sleep, REM - drug effects; Sleep, REM - physiology; Wakefulness - drug effects; Wakefulness - physiology; Reticular formation; Narcolepsy; Autonomic system; HRV; Cholinergic
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2015.05.015

•REM sleep (REMc) and cataplexy (CA) were induced by carbachol injections into the NPO.•HRV was evaluated during these conditions and natural sleep and wakefulness.•Heart rate was greater during CA while LF power was larger during natural REM sleep.•In CA there was a decrease in coupling between the tachogram and respiratory activity.•Although the somatomotor atonia was the same, REMc and CA have differences in the HRV. The nucleus pontis oralis (NPO) exerts an executive control over REM sleep. Cholinergic input to the NPO is critical for REM sleep generation. In the cat, a single microinjection of carbachol (a cholinergic agonist) into the NPO produces either REM sleep (REMc) or wakefulness with muscle atonia (cataplexy, CA). In order to study the central control of the heart rate variability (HRV) during sleep, we conducted polysomnographic and electrocardiogram recordings from chronically prepared cats during REMc, CA as well as during sleep and wakefulness. Subsequently, we performed statistical and spectral analyses of the HRV. The heart rate was greater during CA compared to REMc, NREM or REM sleep. Spectral analysis revealed that the low frequency band (LF) power was significantly higher during REM sleep in comparison to REMc and CA. Furthermore, we found that during CA there was a decrease in coupling between the RR intervals plot (tachogram) and respiratory activity. In contrast, compared to natural behavioral states, during REMc and CA there were no significant differences in the HRV based upon the standard deviation of normal RR intervals (SDNN) and the mean squared difference of successive intervals (rMSSD). In conclusion, there were differences in the HRV during naturally-occurring REM sleep compared to REMc. In addition, in spite of the same muscle atonia, the HRV was different during REMc and CA. Therefore, the neuronal network that controls the HRV during REM sleep can be dissociated from the one that generates the muscle atonia during this state.