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Departments of 1 Psychiatry and the Behavioral Sciences, 2 Neurology, and 3 Cell and Neurobiology, University of Southern California Keck School of Medicine, 4 Department of Molecular Pharmacology and Toxicology, University of Southern California School of Pharmacy, Los Angeles 90089; 5 Greater Los Angeles Veterans Affairs Healthcare System 90073; and 6 Department of Physiology, University of California Los Angeles School of Medicine, Los Angeles, California 90024
Heart rate (HR) dynamics were investigated in mice deficient in monoamine oxidase A and B, whose phenotype includes elevated tissue levels of norepinephrine, serotonin, dopamine, and phenylethylamine. In their home cages, spectral analysis of R-R intervals revealed more pronounced fluctuations at all frequencies in the mutants compared with wild-type controls, with a particular enhancement at 1-4 Hz. No significant genotypic differences in HR variability (HRV) or entropies calculated from Poincaré plots of the R-R intervals were noted. During exposure to the stress of a novel environment, HR increased and HRV decreased in both genotypes. However, mutants, unlike controls, demonstrated a rapid return to baseline HR during the 10-min exposure. Such modulation may result from an enhanced vagal tone, as suggested by the observation that mutants responded to cholinergic blockade with a decrease in HRV and a prolonged tachycardia greater than controls. Monoamine oxidase-deficient mice may represent a useful experimental model for studying compensatory mechanisms responsible for changes in HR dynamics in chronic states of high sympathetic tone.
serotonin; norepinephrine; cholinergic; arrhythmia; heart rate variability; vagus nerve; sympathetic; parasympathetic
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