The etiology of psychopathology is multifaceted and warrants consideration of factors at multiple levels and across developmental time. Although experiences of adversity in early life have been associated with increased risk of developing psychopathology, pathways toward maladaptation or resilience are complex and depend upon a variety of factors, including individuals’ physiological regulation and cognitive functioning. Therefore, in a longitudinal cohort of 113 mother–child dyads, we explored associations from early adverse experiences to physiological coregulation across multiple systems and subsequent variations in executive functioning. Latent profile analysis derived multisystem profiles based on children's heart rate, respiratory sinus arrhythmia, pre-ejection period, and cortisol measured during periods of rest and reactivity throughout a developmentally challenging protocol. Three distinct profiles of multisystem regulation emerged: heightened multisystem baseline activity (anticipatory arousal/ autonomic nervous system [ANS] responder), typically adaptive patterns across all systems (active copers/mobilizers), and heightened hypothalamic–pituitary–adrenal (HPA) axis activity (HPA axis responders). Path models revealed that children exposed to adversity before 18 months were more likely to evidence an anticipatory arousal/ANS responders response at 36 months, and children in this profile had lower executive functioning scores than the active copers/mobilizers. In sum, these findings provide important information about potential physiological associations linking early adversity to variations in children's task-based executive functioning.

While investigating the reversible seasonal obesity of Siberian hamsters, direct sympathetic nervous system (SNS) postganglionic innervation of white adipose tissue (WAT) has been demonstrated using anterograde and retrograde tract tracers. The primary function of this innervation is lipid mobilization. The brain SNS outflow to WAT has been defined using the pseudorabies virus (PRV), a retrograde transneuronal tract tracer. These PRV-labelled SNS outflow neurons are extensively co-localized with melanocortin-4 receptor mRNA, which, combined with functional data, suggests their involvement in lipolysis. The SNS innervation of WAT also regulates fat cell number, as noradrenaline inhibits and WAT denervation stimulates fat cell proliferation in vitro and in vivo respectively. The sensory innervation of WAT has been demonstrated by retrograde tract tracing, electrophysiological recording and labelling of the sensory-associated neuropeptide calcitonin gene-related peptide in WAT. Local injections of the sensory nerve neurotoxin capsaicin into WAT selectively destroy this innervation. Just as surgical removal of WAT pads triggers compensatory increases in lipid accretion by non-excised WAT depots, capsaicin-induced sensory denervation triggers increases in lipid accretion of non-capsaicin-injected WAT depots, suggesting that these nerves convey information about body fat levels to the brain. Finally, parasympathetic nervous system innervation of WAT has been suggested, but the recent finding of no WAT immunoreactivity for the possible parasympathetic marker vesicular acetylcholine transporter (VAChT) argues against this claim. Collectively, these data suggest several roles for efferent and afferent neural innervation of WAT in body fat regulation.

Summary

Background and objective: Desflurane has been shown to increase sympathetic activity and heart rate (HR) in a concentration-dependent manner. Nevertheless, desflurane, like all other volatile anaesthetics, increased HR in parallel to vagal inhibition in a previous study. Therefore, our hypothesis is that desflurane elicits tachycardia by vagal inhibition rather than by activation of the sympathetic nervous system.

Methods: Six dogs were studied awake and during desflurane anaesthesia (1 and 2 MAC) alone, after pre-treatment with propranolol (2 mg kg−1 followed by 1 mg kg−1 h−1), or after pre-treatment with atropine (0.1 mg kg−1 followed by 0.05 mg kg−1 h−1). The effects on HR and HR variability were compared by an analysis of variance (P < 0.05). HR variability was analysed in the frequency domain as power in the high-(0.15–0.5 Hz, vagal activity) and low-frequency range (0.04–0.15 Hz, sympathetic and vagal activity).

Results: HR increased during 2 MAC of desflurane from about 60 (awake) to 118 ± 2 beats min−1 (mean ± SEM) in controls and to 106 ± 3 beats min−1 in dogs pre-treated with propranolol. In contrast, pre-treatment with atropine increased HR from 64 ± 2 to 147 ± 5 beats min−1 (awake) and HR decreased to 120 ± 5 beats min−1 after adding desflurane. High-frequency power correlated inversely with HR (r2 = 0.95/0.93) during desflurane alone and in the presence of β-adrenoceptor blockade, with no significant difference between regression lines. There was no correlation between these variables during atropine/desflurane.

Conclusions: The increase in HR elicited by desflurane mainly results from vagal inhibition and not from sympathetic activation.

We hypothesized that patterns of sympathetic and parasympathetic reactivity observed in adults would be apparent in a sample of children and adolescents and that these patterns would be consistent across tasks. We explored the relationship between these patterns and psychosocial risk factors for cardiovascular disease. We measured preejection period (PEP) and an index of respiratory sinus arrhythmia (mean successive difference [MSD] statistic) during three reactivity tasks. We classified participants into four groups based on increases or decreases in PEP and MSD. Ninety percent of the sample exhibited the same pattern during at least two of the tasks. PEP and MSD demonstrated consistency, suggesting individual response stereotypy. Exhibiting a consistent pattern of decreased PEP and increased MSD was associated with less child- and parent-reported family conflict. These results are discussed in the context of vagal regulation of environmental demands.

Many physiological changes that occur contemporaneously with nausea are mediated by the autonomic nervous system, but the specific autonomic changes associated with nausea have not been characterized. Cardiac parasympathetic (vagal) activity as indicated by heart rate variability, measured as the standard deviation of successive differences (SDSD) in beat-to-beat intervals, was assessed in 24 women with ovarian cancer immediately prior to and accompanying nausea that occurred following anticancer chemotherapy. A progressive increase in SDSD followed infusion of the chemotherapy agent, indicating a rise in cardiac parasympathetic (vagal) activity, with onset of nausea consistently occurring after the peak activity had been reached, at a time when SDSD was decreasing. An increase in parasympathetic activity seems to set the stage for the expression of nausea but an additional stimulus is apparently needed to finally trigger the event.