Concept: Parasympathetic nervous system
Musical performance is a skilled activity performed under intense pressure, thus is often a profound source of anxiety. In other contexts, anxiety and its concomitant symptoms of sympathetic nervous system arousal have been successfully ameliorated with HRV biofeedback (HRV BF), a technique involving slow breathing which augments autonomic and emotional regulatory capacity. Objective: This randomised-controlled study explored the impact of a single 30-minute session of HRV BF on anxiety in response to a highly stressful music performance.
Naturalistic environments have been demonstrated to promote relaxation and wellbeing. We assess opposing theoretical accounts for these effects through investigation of autonomic arousal and alterations of activation and functional connectivity within the default mode network (DMN) of the brain while participants listened to sounds from artificial and natural environments. We found no evidence for increased DMN activity in the naturalistic compared to artificial or control condition, however, seed based functional connectivity showed a shift from anterior to posterior midline functional coupling in the naturalistic condition. These changes were accompanied by an increase in peak high frequency heart rate variability, indicating an increase in parasympathetic activity in the naturalistic condition in line with the Stress Recovery Theory of nature exposure. Changes in heart rate and the peak high frequency were correlated with baseline functional connectivity within the DMN and baseline parasympathetic tone respectively, highlighting the importance of individual neural and autonomic differences in the response to nature exposure. Our findings may help explain reported health benefits of exposure to natural environments, through identification of alterations to autonomic activity and functional coupling within the DMN when listening to naturalistic sounds.
Assessment of anxiety symptoms in autism spectrum disorders (ASD) is a challenging task due to the symptom overlap between the two conditions as well as the difficulties in communication and awareness of emotions in ASD. This motivates the development of a physiological marker of anxiety in ASD that is independent of language and does not require observation of overt behaviour. In this study, we investigated the feasibility of using indicators of autonomic nervous system (ANS) activity for this purpose. Specially, the objectives of the study were to 1) examine whether or not anxiety causes significant measurable changes in indicators of ANS in an ASD population, and 2) characterize the pattern of these changes in ASD. We measured three physiological indicators of the autonomic nervous system response (heart rate, electrodermal activity, and skin temperature) during a baseline (movie watching) and anxiety condition (Stroop task) in a sample of typically developing children (n = 17) and children with ASD (n = 12). The anxiety condition caused significant changes in heart rate and electrodermal activity in both groups, however, a differential pattern of response was found between the two groups. In particular, the ASD group showed elevated heart rate during both baseline and anxiety conditions. Elevated and blunted phasic electrodermal activity were found in the ASD group during baseline and anxiety conditions, respectively. Finally, the ASD group did not show the typical decrease in skin temperature in response to anxiety. These results suggest that 1) signals of the autonomic nervous system may be used as indicators of anxiety in children with ASD, and 2) ASD may be associated with an atypical autonomic response to anxiety that is most consistent with sympathetic over-arousal and parasympathetic under-arousal.
Imbalances of energy homeostasis are often associated with cardiovascular complications. Previous work has shown that Gnasxl deficient mice have a lean and hypermetabolic phenotype with increased sympathetic stimulation of adipose tissue. The Gnasxl transcript from the imprinted Gnas locus encodes the trimeric G-protein subunit XLαs, which is expressed in brain regions that regulate energy homeostasis and sympathetic nervous system (SNS) activity. To determine whether Gnasxl knock-out (KO) mice display additional SNS related phenotypes, we have now investigated the cardiovascular system. Gnasxl KO mice were ≈20 mmHg hypertensive compared to wild-type (WT) littermates (p≤0.05) and hypersensitive to the sympatholytic drug reserpine. Using telemetry, we detected an increased waking heart rate (HR) in conscious KOs (630±10 vs 584±12 bpm, KO vs WT, p≤0.05). Body temperature was also elevated (38.1±0.3 vs 36.9±0.4 °C, KO vs WT, p≤0.05). To investigate autonomic nervous system influences, we used heart rate variability (HRV) analyses. We empirically defined frequency power bands using atropine and reserpine and verified high frequency (HF) power and low frequency (LF) LF/HF power ratio to be indicators of parasympathetic and sympathetic activity, respectively. LF/HF power ratio was greater in KOs and more sensitive to reserpine than in WTs, consistent with elevated SNS activity. By contrast, atropine and exendin-4 (Ex-4), a centrally acting agonist of the glucagon-like peptide-1 (GLP-1) receptor, which influences cardiovascular physiology and metabolism, reduced HF power equally in both genotypes. This was associated with a stronger increase in HR in KOs. Mild stress had a blunted effect on LF/HF ratio in KOs consistent with elevated basic sympathetic activity. We conclude that XLαs is required for the inhibition of sympathetic outflow towards cardiovascular and metabolically relevant tissues.
To determine if potential biomarkers can be used to identify subgroups of people with irritable bowel syndrome (IBS) who will benefit the most or the least from a comprehensive self-management (CSM) intervention.
The parasympathetic nervous system plays an important role in the pathophysiology of atrial fibrillation. Catheter ablation, a minimally invasive procedure deactivating abnormal firing cardiac tissue, is increasingly becoming the therapy of choice for atrial fibrillation. This is inevitably associated with the obliteration of cardiac cholinergic neurons. However, the impact on ventricular electrophysiology is unclear. Here we show that cardiac cholinergic neurons modulate ventricular electrophysiology. Mechanical disruption or pharmacological blockade of parasympathetic innervation shortens ventricular refractory periods, increases the incidence of ventricular arrhythmia and decreases ventricular cAMP levels in murine hearts. Immunohistochemistry confirmed ventricular cholinergic innervation, revealing parasympathetic fibres running from the atria to the ventricles parallel to sympathetic fibres. In humans, catheter ablation of atrial fibrillation, which is accompanied by accidental parasympathetic and concomitant sympathetic denervation, raises the burden of premature ventricular complexes. In summary, our results demonstrate an influence of cardiac cholinergic neurons on the regulation of ventricular function and arrhythmogenesis.
Developments in information technology cause a great deal of stress to modern people, and controlling this stress now becomes an important issue. The aim of this study was to examine psychological and physiological benefits of interaction with indoor plants.
It is generally accepted that gamma-aminobutyric acid (GABA) is a signaling molecule abundant in central synapses. In a number of studies though, it has been shown that GABA signaling functions in the peripheral nervous system as well, in particular, in the synapses of sympathetic ganglia. However, there exists no firm evidence on the presence of GABAergic signaling cascade in the intercellular junctions of the somatic nerve system. By the use of immunohistochemistry methods, in the synaptic area of cholinergic neuromuscular contact in rat diaphragm, we have detected glutamate decarboxylase, the enzyme involved in synthesis of GABA, molecules of GABA, and also GAT-2, a protein responsible for transmembrane transport of GABA. Earlier we have also shown that metabotropic GABABreceptors have overlapping localization in the same compartment. Moreover, activation of GABABreceptors affects the intensity of acetylcholine release. These data taken together, allows us to suggest that in the mammalian cholinergic neuromuscular junction, GABA is synthesized and performs certain synaptic signaling function.
An unusual, but common, aversion to images with clusters of holes is known as trypophobia. Recent research suggests that trypophobic reactions are caused by visual spectral properties also present in aversive images of evolutionary threatening animals (e.g., snakes and spiders). However, despite similar spectral properties, it remains unknown whether there is a shared emotional response to holes and threatening animals. Whereas snakes and spiders are known to elicit a fear reaction, associated with the sympathetic nervous system, anecdotal reports from self-described trypophobes suggest reactions more consistent with disgust, which is associated with activation of the parasympathetic nervous system. Here we used pupillometry in a novel attempt to uncover the distinct emotional response associated with a trypophobic response to holes. Across two experiments, images of holes elicited greater constriction compared to images of threatening animals and neutral images. Moreover, this effect held when controlling for level of arousal and accounting for the pupil grating response. This pattern of pupillary response is consistent with involvement of the parasympathetic nervous system and suggests a disgust, not a fear, response to images of holes. Although general aversion may be rooted in shared visual-spectral properties, we propose that the specific emotion is determined by cognitive appraisal of the distinct image content.
The return trip often seems shorter than the outward trip even when the distance and actual time are identical. To date, studies on the return trip effect have failed to confirm its existence in a situation that is ecologically valid in terms of environment and duration. In addition, physiological influences as part of fundamental timing mechanisms in daily activities have not been investigated in the time perception literature. The present study compared round-trip and non-round-trip conditions in an ecological situation. Time estimation in real time and postdictive estimation were used to clarify the situations where the return trip effect occurs. Autonomic nervous system activity was evaluated from the electrocardiogram using the Lorenz plot to demonstrate the relationship between time perception and physiological indices. The results suggest that the return trip effect is caused only postdictively. Electrocardiographic analysis revealed that the two experimental conditions induced different responses in the autonomic nervous system, particularly in sympathetic nervous function, and that parasympathetic function correlated with postdictive timing. To account for the main findings, the discrepancy between the two time estimates is discussed in the light of timing strategies, i.e., prospective and retrospective timing, which reflect different emphasis on attention and memory processes. Also each timing method, i.e., the verbal estimation, production or comparative judgment, has different characteristics such as the quantification of duration in time units or knowledge of the target duration, which may be responsible for the discrepancy. The relationship between postdictive time estimation and the parasympathetic nervous system is also discussed.