Arousal Control Research Articles

Interoception, emotion regulation strategies and skin-picking behaviors – Results of an intensive longitudinal study

Compulsive skin-picking is associated with emotion regulation difficulties, whose origins remain unclear. Interoception, plays an important role in effective emotion regulation. This study examined the relationship between interoception, emotion regulation strategies, and skin-picking in 136 individuals (85% women, aged 18–41), including 71 engaging in skin-picking and 65 psychologically healthy controls. We were interested in between-group differences in maladaptive and adaptive emotion regulation and aspects of interoception as well as associations of the latter with skin-picking symptoms and use of emotion regulation strategies. At baseline, we assessed habitual emotion regulation strategies (rumination, suppression, distraction, engagement, arousal control, reappraisal) and Interoceptive Sensibility (e.g., emotional awareness, body listening, self-regulation, noticing) through self-report questionnaires. Moreover, Interoceptive Accuracy (IAc) was measured via a Heartbeat Counting Task. Additionally, Ecological Momentary Assessment (EMA) over seven days was used to register use of emotion regulation strategies and the occurrence and severity of skin-picking episodes during that period. At baseline, the skin-picking group exhibited lower IAc, emotional awareness, and higher habitual use of rumination than control group. Lower IAc was associated with higher odds of reporting skin-picking episodes assessed during EMA. Body listening correlated with a reduced sense of control over skin-picking during EMA. In total sample, self-regulation was related to lower odds of using rumination during EMA and noticing with less use of cognitive reappraisal. The study highlights the complex relationship between interoception, emotion regulation, and skin-picking, offering new insights into the mechanisms underlying skin picking disorder.

A network approach to emotion regulation and symptom activation in depression and anxiety.

Emotions can be regulated through several regulatory strategies that are involved in the development of psychopathological symptoms. Despite the well-established association between psychopathology and emotion dysregulation, little is known about the relationship between individual symptoms of depression and anxiety and emotion regulation strategies (ERS), as well as between ERS themselves. We conducted a cross-sectional study and examined the interactions between six ERS (reappraisal, engagement, rumination, suppression, arousal control, and distraction) and assessed their distinctive association with the activation of specific symptoms of depression and anxiety in a community sample of 376 adults (80.4% female; Mage = 32.70; SDage = 11.80). The Regulation Emotion Systems Survey (RESS) was used to measure ERS. The Patient Health Questionnaire (PHQ-9) and the Generalized Anxiety Disorder (GAD-7) were used to assess psychological symptoms. An exploratory graph analysis was performed to examine the structural properties of the network of interactions between these behaviors. Additionally, to test the association of ERS with the activation of the depression symptoms network, an expected symptoms activity (ESA) was conducted. Six communities were found that correspond to the six ERS. Rumination and suppression have a significant association with symptom activation (particularly low self-esteem), whereas reappraisal reduces symptomatic activation. The effect of arousal control, engagement, and distraction appears to depend on the remaining ERS rather than having much influence on their own. This study provides insight into how ERS interact with each other and with individual symptoms of depression and anxiety. Understanding the effects of these interactions on symptom activation and comorbidity can improve our understanding of psychopathology.

Bidirectional brain-body interactions during natural story listening

Narratives can synchronize neural and physiological signals between individuals, but the relationship between these signals, and the underlying mechanism, is unclear. We hypothesized a top-down effect of cognition on arousal and predicted that auditory narratives will drive not only brain signals but also peripheral physiological signals. We find that auditory narratives entrained gaze variation, saccade initiation, pupil size, and heart rate. This is consistent with a top-down effect of cognition on autonomic function. We also hypothesized a bottom-up effect, whereby autonomic physiology affects arousal. Controlled breathing affected pupil size, and heart rate was entrained by controlled saccades. Additionally, fluctuations in heart rate preceded fluctuations of pupil size and brain signals. Gaze variation, pupil size, and heart rate were all associated with anterior-central brain signals. Together, these results suggest bidirectional causal effects between peripheral autonomic function and central brain circuits involved in the control of arousal.

Predicting performance of elite kickboxers using the multi‐states theory framework

AbstractUsing the multi‐states (MuSt) theory framework, this study examined the interplay between self‐confidence, emotional arousal control, worry, concentration disruption, challenge and threat appraisals, psychobiosocial experiences, and self‐evaluated performance of medalist kickboxers involved in the WAKO World Kickboxing Championship 2021. Participants were 103 gold, silver, or bronze medalists (58 women and 45 men), aged 18–39 (M = 25.16 ± 4.54 years), who were contacted via email and social media and asked to fill an online survey 3 months after the event. According to the MuSt theory predictions, self‐confidence and emotional arousal control were positively related to challenge appraisal, functional psychobiosocial experiences, and self‐evaluated performance. Worry and concentration disruption were positively associated with threat appraisal, and negatively related to functional psychobiosocial experiences; concentration disruption was also negatively related to self‐evaluated performance. Results from path analysis revealed a positive indirect link from self‐confidence to self‐evaluated performance via challenge appraisal and psychobiosocial experiences. Negative indirect links from worry and concentration disruption to self‐evaluated performance through threat appraisal and psychobiosocial experiences were significant. A positive indirect effect from emotional arousal control to self‐evaluated performance via psychobiosocial experiences was also shown. The findings are discussed in light of the MuSt theory.

From active affordance to active inference: vertical integration of cognition in the cerebral cortex through dual subcortical control systems.

In previous papers, we proposed that the dorsal attention system's top-down control is regulated by the dorsal division of the limbic system, providing a feedforward or impulsive form of control generating expectancies during active inference. In contrast, we proposed that the ventral attention system is regulated by the ventral limbic division, regulating feedback constraints and error-correction for active inference within the neocortical hierarchy. Here, we propose that these forms of cognitive control reflect vertical integration of subcortical arousal control systems that evolved for specific forms of behavior control. The feedforward impetus to action is regulated by phasic arousal, mediated by lemnothalamic projections from the reticular activating system of the lower brainstem, and then elaborated by the hippocampus and dorsal limbic division. In contrast, feedback constraint-based on environmental requirements-is regulated by the tonic activation furnished by collothalamic projections from the midbrain arousal control centers, and then sustained and elaborated by the amygdala, basal ganglia, and ventral limbic division. In an evolutionary-developmental analysis, understanding these differing forms of active affordance-for arousal and motor control within the subcortical vertebrate neuraxis-may help explain the evolution of active inference regulating the cognition of expectancy and error-correction within the mammalian 6-layered neocortex.

Continuity and change in neural plasticity through embryonic morphogenesis, fetal activity-dependent synaptogenesis, and infant memory consolidation.

There is an apparent continuity in human neural development that can be traced to venerable themes of vertebrate morphogenesis that have shaped the evolution of the reptilian telencephalon (including both primitive three-layered cortex and basal ganglia) and then the subsequent evolution of the mammalian six-layered neocortex. In this theoretical analysis, we propose that an evolutionary-developmental analysis of these general morphogenetic themes can help to explain the embryonic development of the dual divisions of the limbic system that control the dorsal and ventral networks of the human neocortex. These include the archicortical (dorsal limbic) Papez circuits regulated by the hippocampus that organize spatial, contextual memory, as well as the paleocortical (ventral limbic) circuits that organize object memory. We review evidence that these dorsal and ventral limbic divisions are controlled by the differential actions of brainstem lemnothalamic and midbrain collothalamic arousal control systems, respectively, thereby traversing the vertebrate subcortical neuraxis. These dual control systems are first seen shaping the phyletic morphogenesis of the archicortical and paleocortical foundations of the forebrain in embryogenesis. They then provide dual modes of activity-dependent synaptic organization in the active (lemnothalamic) and quiet (collothalamic) stages of fetal sleep. Finally, these regulatory systems mature to form the major systems of memory consolidation of postnatal development, including the rapid eye movement (lemnothalamic) consolidation of implicit memory and social attachment in the first year, and then-in a subsequent stage-the non-REM (collothalamic) consolidation of explicit memory that is integral to the autonomy and individuation of the second year of life.

Self-regulating arousal via pupil-based biofeedback

The brain’s arousal state is controlled by several neuromodulatory nuclei known to substantially influence cognition and mental well-being. Here we investigate whether human participants can gain volitional control of their arousal state using a pupil-based biofeedback approach. Our approach inverts a mechanism suggested by previous literature that links activity of the locus coeruleus, one of the key regulators of central arousal and pupil dynamics. We show that pupil-based biofeedback enables participants to acquire volitional control of pupil size. Applying pupil self-regulation systematically modulates activity of the locus coeruleus and other brainstem structures involved in arousal control. Furthermore, it modulates cardiovascular measures such as heart rate, and behavioural and psychophysiological responses during an oddball task. We provide evidence that pupil-based biofeedback makes the brain’s arousal system accessible to volitional control, a finding that has tremendous potential for translation to behavioural and clinical applications across various domains, including stress-related and anxiety disorders.

A common thalamic hub for general and defensive arousal control

The expression of defensive responses to alerting sensory cues requires both general arousal and a specific arousal state associated with defensive emotions. However, it remains unclear whether these two forms of arousal can be regulated by common brain regions. We discovered that the medial sector of the auditory thalamus (ATm) in mice is a thalamic hub controlling both general and defensive arousal. The spontaneous activity of VGluT2-expressing ATm (ATmVGluT2+) neurons was correlated with and causally contributed to wakefulness. In sleeping mice, sustained ATmVGluT2+ population responses were predictive of sensory-induced arousal, the likelihood of which was markedly decreased by inhibiting ATmVGluT2+ neurons or multiple downstream pathways. In awake mice, ATmVGluT2+ activation led to heightened arousal accompanied by excessive anxiety and avoidance behavior. Notably, blocking their neurotransmission abolished alerting stimuli-induced defensive behaviors. These findings may shed light on the comorbidity of sleep disturbances and abnormal sensory sensitivity in specific brain disorders.

Is cortisol an endogenous mediator of erectile dysfunction in the adult male?

It has been speculated for decades whether there is a significance of the adrenal corticosteroid cortisol in the process of male sexual function, including the control of sexual arousal and penile erection. In order to investigate further the role of the adrenocorticotropic axis in the physiological process of penile erection, we aimed to determine the course of cortisol in the cavernous and systemic blood through different stages of sexual arousal in patients suffering from erectile dysfunction (ED) in comparison to a cohort of healthy males. Fifty-four healthy adult males and 45 patients with ED were presented sexually explicit visual material in order to elicit tumescence and (in the healthy males) rigid erection. Blood was collected from the cavernous space (corpus cavernosum penis, CC) and a cubital vein (CV) at different stages of the sexual arousal cycle as indicated by the penile stages flaccidity, tumescence, rigidity (attained only by the healthy males) and detumescence. Cortisol (µg/dL serum) was measured using a radioimmunometric assay (RIA). In healthy males, cortisol decreased in both the cavernous and systemic blood with the beginning of sexual stimulation (CV: 15 to 13, CC: 16 to 13). At detumescence, in the systemic circulation, no alterations in cortisol levels were registered, whereas it decreased further in the CC (to 12). In the ED patients, no significant changes in cortisol were noticed in the systemic and cavernous blood. The findings indicate that cortisol might act as an antagonist of the normal sexual response cycle of the adult male. A dysregulation of the secretion and/or degradation of the hormone might well play a role in the manifestation of ED.

What Is the Involvement of the Cerebellum During Sleep?

Compared with the advances in the elucidation of the role of brainstem and hypothalamus in the control of wakefulness and sleep stages,1 the functions of the cerebellum during sleep remain relatively unexplored.2 However, the activity in the cerebellum changes concomitantly with that of the neocortex during distinct sleep stages, as shown, for example, with a simultaneous recoding of sleep EEG and regional blood flow or fMRI signals in the cerebellum in humans.2-10 Electrophysiologic studies show variation in the firing rate of Purkinje and cerebellar nuclear cells according to the neocortical sleep stage.11-15 Recent studies show hippocampal-cerebellar interactions both during non-REM (NREM) and REM sleep16 and suggest a cerebellar contribution to the generation of sleep spindles in the neocortex.15 There are several potential pathways for the coordination of neocortical or hippocampal regions with cerebellar activity during sleep (Figure). This reciprocal communication may provide a potential basis for the consolidation of motor learning and other cognitive functions.17-22 The cerebellum is affected in several disorders associated with sleep disturbances.23-25 However, the contribution of the cerebellum to the normal regulation of sleep and its role in sleep disorders are still incompletely understood. Elucidating the role of the cerebellum in the control of arousal and sleep-wake cycle has potential clinical and therapeutic implications.

Orexinergic neurons modulate stress coping responses in mice.

Stress is a critical precipitating factor for major depression. However, individual responses to the same stressor vary widely, possibly owing to individual variations in stress resilience. Nevertheless, the factors that determine stress susceptibility and resilience remain poorly understood. Orexin neurons have been implicated in the control of stress-induced arousal. Therefore, we investigated whether orexin-expressing neurons are involved in the regulation of stress resilience in male mice. We found that the level of c-fos expression was significantly different in susceptible versus resilient mice in the learned helplessness test (LHT). Furthermore, activating orexinergic neurons induced resilience in the susceptible group, and this resilience was also consistently observed in other behavioral tests. However, activating orexinergic neurons during the induction period (during inescapable stress exposure) did not affect stress resilience in the escape test. In addition, analyses using pathway-specific optic stimulation revealed that activating orexinergic projections to the medial part of the nucleus accumbens (NAc) alone mediated a decrease in anxiety but was not sufficient to induce resilience in the LHT. Collectively, our data suggest that orexinergic projections to multiple targets control diverse and flexible stress-related behaviors in response to various stressors.

Paraventricular thalamus controls consciousness transitions during propofol anaesthesia in mice

BackgroundThe neuronal mechanisms underlying propofol-induced modulation of consciousness are poorly understood. Neuroimaging studies suggest a potential role for non-specific thalamic nuclei in propofol-induced loss of consciousness. We investigated the contribution of the paraventricular thalamus (PVT), a midline thalamic nucleus that has been implicated in arousal control and general anaesthesia with inhaled anaesthetics, to loss and recovery of consciousness during propofol anaesthesia. MethodsPolysomnographic recordings and righting reflex test were used to determine the transitions of loss and recovery of righting reflex, used as a measure of consciousness in mice, during propofol anaesthesia in mice under conditions mimicking clinical propofol administration. PVT neuronal activities were monitored using fibre photometry and regulated using optogenetic and chemogenetic methods. ResultsPopulation activities of PVT glutamatergic neurones began to decrease before propofol-induced loss of consciousness and rapidly increased to a peak at the onset of recovery of consciousness. Chemogenetic inhibition of PVT calretinin-expressing (PVTCR) neurones shortened onset (from 176 [35] to 127 [26] s; P=0.001) and prolonged return (from 1568 [611] to 3126 [1616] s; P=0.002) of righting reflex. Conversely, chemogenetic activation of PVTCR neurones exerted opposite effects. Furthermore, optogenetic silencing of PVTCR neurones accelerated transitions to loss of consciousness (from 205 [35] to 158 [44] s; P=0.027) and slowed transitions to recovery of consciousness (from 230 [78] to 370 [99] s; P=0.041). During a steady period of unconsciousness maintained with continuous propofol infusion, brief optical activation of PVTCR neurones restored cortical activity and arousal with a latency of about 5 s. ConclusionsThe paraventricular thalamus contributes to the control of consciousness transitions in propofol anaesthesia in mice. This provides a potential neuroanatomical target for controlling consciousness to reduce anaesthetic dose requirements and side effects.

Low Levels of Adenosine and GDNF Are Potential Risk Factors for Parkinson's Disease with Sleep Disorders.

Sleep disturbances are the most prevalent non-motor symptoms in the preclinical stage of Parkinson's disease (PD). Adenosine, glial-derived neurotrophic factor (GDNF), and associated neurotransmitters are crucial in the control of sleep arousal. This study aimed to detect the serum levels of adenosine, GDNF, and associated neurotransmitters and explored their correlations with PD with sleep disorders. Demographic characteristics and clinical information of PD patients and healthy participants were assessed. Serum concentrations of adenosine, GDNF, and related neurotransmitters were detected by ELISA and LC-MS. The correlation between serum levels of adenosine, GDNF, and associated neurotransmitters and sleep disorders was explored using logistic regression. PD patients with sleep disorders had higher scores of HAMA, HAMD, ESS, UPDRS-III, and H-Y stage. Lower levels of adenosine, GDNF, and γ-GABA were observed in PD patients who had sleep problems. Logistic regression analysis showed adenosine and GDNF were protective factors for preventing sleep disorders. Adenosine combined with GDNF had a higher diagnostic efficiency in predicting PD with sleep disorders by ROC analysis. This study revealed low adenosine and GDNF levels may be risk factors for sleep disorders in PD. The decrease of serum adenosine and GDNF levels may contribute to the diagnosis of PD with sleep disturbances.

On shame and the perceived credibility of sexual assault allegations

AbstractDespite the high incidence of sexual assault, doubt about allegations is common. Previous research suggests that victims expressing positive or no emotion are perceived as less credible than those expressing negative emotions. However, little is known about which specific negative emotional expressions contribute to credibility in this context. In two studies (N = 623), participants read a date rape vignette. The alleged victim's statement was paired with a picture of a female person expressing either shame, sadness, or no emotion. Participants rated the credibility of her account and completed a measure of rape myth acceptance. Controlling for rape myth acceptance, allegations were perceived as more credible when accompanied by an expression of shame versus sadness (a negative, low arousal control condition). It is critical to be aware of the shame‐credibility bias in this context to intervene and support those who have experienced sexual assault.

Perceptual richness of words and its role in free and cued recall

This research aimed to clarify the role of the perceptual richness of words (PR) in the recall tasks. PR was operationalized as the number of sensory modalities through which an object can be perceived. Previously, we found that concepts experienced with many modalities (dog) were recalled more accurately in cued recall than those perceived with few modalities (rainbow) and abstract words. This finding fitted the Perceptual symbol system theory (PSST) and the Dual coding theory (DCT) predictions. We tested the PR effect in both cued (experiment 1- E1) and free recall tasks (experiment 2 – E2) in the present study. With careful stimuli manipulation of context availability and emotional valence and statistical control of arousal and relatedness, made to exclude their influence on recall, we tested alternative explanations of the concreteness effect offered by the relational-distinctiveness hypothesis. The additional perceptual codes improved recall accuracy in the cued recall task (E1), which was in line with the PSST and the DCT. This conclusion is straightforward: two critical groups of concrete words were matched for concreteness and visual perceptual strength. Thus, more accurate recall of concepts experienced with many modalities can be attributed to richer perceptual experience. However, the relational information was essential for recall accuracy in the free recall task (E2), as hypothesized by the relational-distinctiveness hypothesis.

Individual differences in working memory capacity, attention control, fluid intelligence, and pupillary measures of arousal.

The present study examined individual differences in 3 cognitive abilities: attention control (AC), working memory capacity (WMC), and fluid intelligence (gF) as they relate the tendency to experience task-unrelated thoughts (TUTs) and the regulation of arousal. Cognitive abilities were measured with a battery of 9 laboratory tasks, TUTs were measured via thought probes inserted into 2 tasks, and arousal regulation was measured via pupillometry. Recent theorizing (Unsworth & Robison, 2017b) suggests that 1 reason why some people experience relatively frequent TUTs and relatively poor cognitive performance-especially AC and WMC-is that they exhibit dysregulated arousal. Here, we examined how arousal regulation might predict both AC and WMC, but also higher-order cognitive abilities like gF. Further, we examine direct and indirect associations with these abilities via a mediating influence of TUT. Participants who reported more TUTs also tended to exhibit poorer AC, lower WMC, and lower gF. Arousal dysregulation correlated with more TUTs and lower AC. However, there was no direct correlation between arousal regulation and WMC, nor between arousal regulation and gF. The association between arousal regulation and gF was indirect via TUT. We discuss the implications of the results in light of the arousal regulation theory of individual differences and directions for future research. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Catecholaminergic innervation and D2-like dopamine receptor-mediated modulation of brainstem nucleus incertus neurons in the rat

Nucleus incertus (NI) is a brainstem structure involved in the control of arousal, stress responses and locomotor activity. It was reported recently that NI neurons express the dopamine type 2 (D2) receptor that belongs to the D2-like receptor (D2R) family, and that D2R activation in the NI decreased locomotor activity. In this study, using multiplex in situ hybridization, we observed that GABAergic and glutamatergic NI neurons express D2 receptor mRNA, and that D2 receptor mRNA-positive neurons belong to partially overlapping relaxin-3- and cholecystokinin-positive NI neuronal populations. Our immunohistochemical and viral-based retrograde tract-tracing studies revealed a dense innervation of the NI area by fibers containing the catecholaminergic biosynthesis enzymes, tyrosine hydroxylase (TH) and dopamine β-hydroxylase (DBH), and indicated the major sources of the catecholaminergic innervation of the NI as the Darkschewitsch, raphe and hypothalamic A13 nuclei. Furthermore, using whole-cell patch clamp recordings, we demonstrated that D2R activation by quinpirole produced excitatory and inhibitory influences on neuronal activity in the NI, and that both effects were postsynaptic in nature. Moreover, the observed effects were cell-type specific, as type I NI neurons were either excited or inhibited, whereas type II NI neurons were mainly excited by D2R activation. Our results reveal that rat NI receives a strong catecholaminergic innervation and suggest that catecholamines acting within the NI are involved in the control of diverse processes, including locomotor activity, social interaction and nociceptive signaling. Our data also strengthen the hypothesis that the NI acts as a hub integrating arousal-related neuronal information.

It's Time to Talk About Fear.

It's Time to Talk About Fear.

Neuroanatomical Basis for the Orexinergic Modulation of Anesthesia Arousal and Pain Control.

Hypothalamic orexin (hypocretin) neurons play crucial roles in arousal control. Their involvement in anesthesia and analgesia remains to be better understood. In order to enhance our view on the neuroanatomy, we systematically mapped the projections of orexin neurons with confocal microscope and light sheet microscope. We specifically expressed optogenetic opsins tagged with fluorescence markers in orexin neurons through adeno-associated viral infection in the mouse brain. The imaging results revealed fine details and novel features of the orexin projections throughout the brain, particularly related to the nuclei regulating arousal and pain. We then optogenetically activated orexin neurons in the lateral hypothalamus to study the effects on anesthesia-related behaviors. cFos staining showed that optogenetic stimulation can activate orexin neurons in the ChR2-mCherry group, but not the control mCherry group (62.86 ± 3.923% vs. 7.9 ± 2.072%; P < 0.0001). In behavior assays, optogenetic stimulation in the ChR2-mCherry group consistently elicited robust arousal from light isoflurane anesthesia (9.429 ± 3.804 s vs. 238.2 ± 17.42 s; P < 0.0001), shortened the emergence time after deep isoflurane anesthesia (109.5 ± 13.59 s vs. 213.8 ± 21.77 s; P = 0.0023), and increased the paw withdrawal latency in a hotplate test (11.45 ± 1.185 s vs. 8.767 ± 0.7775; P = 0.0317). The structural details of orexin fibers established the neuroanatomic basis for studying the role of orexin in anesthesia and analgesia.

Control of Behavioral Arousal and Defense by a Glutamatergic Midbrain-Amygdala Pathway in Mice.

In response to external threatening signals, animals evolve a series of defensive behaviors that depend on heightened arousal. It is believed that arousal and defensive behaviors are coordinately regulated by specific neurocircuits in the central nervous system. The ventral tegmental area (VTA) is a key structure located in the ventral midbrain of mice. The activity of VTA glutamatergic neurons has recently been shown to be closely related to sleep–wake behavior. However, the specific role of VTA glutamatergic neurons in sleep–wake regulation, associated physiological functions, and underlying neural circuits remain unclear. In the current study, using an optogenetic approach and synchronous polysomnographic recording, we demonstrated that selective activation of VTA glutamatergic neurons induced immediate transition from sleep to wakefulness and obviously increased the amount of wakefulness in mice. Furthermore, optogenetic activation of VTA glutamatergic neurons induced multiple defensive behaviors, including burrowing, fleeing, avoidance and hiding. Finally, viral-mediated anterograde activation revealed that projections from the VTA to the central nucleus of the amygdala (CeA) mediated the wake- and defense-promoting effects of VTA glutamatergic neurons. Collectively, our results illustrate that the glutamatergic VTA is a key neural substrate regulating wakefulness and defensive behaviors that controls these behaviors through its projection into the CeA. We further discuss the possibility that the glutamatergic VTA-CeA pathway may be involved in psychiatric diseases featuring with excessive defense.