Aim: 

Stress-related psychopathologies such as anxiety and depression and cardiovascular morbidity seem to share a number of biological substrates, including central serotonergic dysfunction and autonomic inbalance. Previous studies indicated that the activation of central 5-HT_1A receptors attenuates heart rate and blood pressure raises during stress, supporting a crucial role of these receptors in moderating sympathetic activation. This study evaluated cardiac sympathovagal modulation in mice lacking 5-HT_1A receptors and exposed to different stressors.

Methods: 

Male KO (N=6) and WT (N=6) mice were implanted with transmitters for ECG recordings and subjected to chronic social stress (CSS, 15-day adverse sensory contact with an aggressive male and defeat episodes on day 1, 2, 3, 8, and 15). Before CSS, mice were injected with 8-OH-DPAT, a 5-HT_1A agonist. Before and after CSS, they were exposed to restraint test.

Results: 

Following 8-OH-DPAT administration and during the two restraint tests, KOs exhibited higher heart rates and lower values of vagal activity index, though they did not differ from WTs in cardiac reactivity during defeat episodes. CSS determined a reduction in the amplitude of HR rhythm that was larger in KO mice.

Conclusion: 

These results suggest that the deletion of 5-HT_1A receptors accentuates tachycardia and dampens vagal modulation of heart rate during non-social stressors, and increases the susceptibility to alterations in circadian rhythmicity of heart rate during a chronic social challenge.