Premium
Cardiorespiratory control as a function of wake‐sleep behavior and diet in mice lacking CB 1 cannabinoid receptors
Author(s) -
Silvani Alessandro,
Bastianini Stefano,
Berteotti Chiara,
Cohen Gary,
Martire Viviana Lo,
Mazza Roberta,
Quarta Carmelo,
Pagotto Uberto,
Zoccoli Giovanna
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.926.1
Subject(s) - cardiorespiratory fitness , endocrinology , medicine , sleep (system call) , endocannabinoid system , blood pressure , respiratory system , heart rate , cannabinoid receptor , cannabinoid , plethysmograph , receptor , antagonist , computer science , operating system
Cannabinoid type 1 receptors (CB 1 R) are widely expressed in the brain. We investigated the effects of chronic CB 1 R deficiency on cardiorespiratory control as a function of wake‐sleep behavior and diet. Adult male CB 1 R knock‐out (KO) and wild‐type (WT) control mice (n=9–10 per group) were fed standard diet or HFD for 3 months and instrumented with electrodes and a telemetric blood pressure (BP) transducer. Sleep was recorded with either BP and heart rate (HR) or ventilation (whole‐body plethysmography). We found that KO slept less than WT during the dark (active) period and retained clear‐cut effects of sleep on cardiovascular and respiratory control. HFD increased HR in KO and WT. KO fed HFD had higher values of BP and HR during the dark period and more frequent apneas during non‐rapid‐eye‐movement sleep than WT. These results suggest that CB 1 R are not necessary for the occurrence of sleep‐dependent cardiovascular and respiratory changes. However, CB 1 R are necessary for physiological control of wake‐sleep behavior and of respiratory variability during sleep. Finally, chronic lack of endocannabinoid signaling through CB 1 R may enhance cardiovascular consequences of HFD. This effect is of interest because lack of CB 1 R signaling has been shown to protect from metabolic derangements induced by HFD by increasing sympathetic activity to brown adipose tissue.