A Neural Systems Approach to the Study of the Respiratory-Type Panic Disorder

Schenberg, Luiz Carlos

doi:10.1007/978-3-319-12538-1_2

Cited by 9 publications

(7 citation statements)

References 429 publications

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“…For instance, the RCF could evoke microglia-mediated acid-sensing activity or neuro-inflammatory responses (Vollmer et al, 2016), and alter acid-base regulation and chemosensory mechanisms (Tay et al, 2017) that are being hypothesized and investigated in laboratory and clinical studies of PD and AD. Indeed, evidence in favor of increased brain lactate and extracellular brain acidification in PD is offered by human functional brain imaging studies (Maddock et al, 2013; Magnotta et al, 2012), and translational models of PD in rodents focused on chemosensory mechanisms and acid–base dysregulation (D’Amato et al, 2011; Leibold et al, 2016) are therefore particularly timely (Schenberg, 2016).…”

Section: Discussionmentioning

confidence: 99%

Amiloride modulation of carbon dioxide hypersensitivity and thermal nociceptive hypersensitivity induced by interference with early maternal environment

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Amiloride modulation of carbon dioxide hypersensitivity and thermal nociceptive hypersensitivity induced by interference with early maternal environment

et al. 2018

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“…That said, several additional structures could have been investigated. Amongst those, periaqueductal grey matter (PAG) is worth noting because it is considered as the final common pathway of all defensive behaviours (including respiratory responses) and therefore plays an important role in the mediation of panic attacks . Thus, the PAG could be an alternative explanation for the results reported in the present study.…”

Section: Discussionmentioning

confidence: 68%

“…The rapid increase in arterial Pco 2 that follows CO 2 inhalation activates chemosensors among the periphery and brain, which then initiate robust hyperventilation. The CO 2 chemosensory circuit is an important aspect in PD pathophysiology; when chemosensitivity and/or responsiveness to CO 2 become excessive, physiological and emotional responses associated with fear and panic are observed . The carotid bodies are mainly known for their ability to sense O 2 in arterial blood; however, these peripheral chemoreceptors also contribute significantly to the HCVR and their activation by potassium cyanide injection (i.v.)…”

Section: Discussionmentioning

confidence: 99%

“…For a subpopulation of PD patients, respiratory manifestations are a hallmark of this disorder. Symptoms include intense air hunger, shortness of breath and hyperventilation . The pathophysiological mechanism triggering the occurrence of panic attacks involves complex, inter‐related processes.…”

Section: Introductionmentioning

confidence: 99%

“…On the other hand, the fact that panic attacks and PD diagnosis emerge at puberty and also show a higher prevalence in women strongly suggests that neuroendocrine disruption also contributes to the pathophysiology . Despite recent progress in our understanding of PD, the lack of proper animal models reproducing these two aspects of the disease impedes progress.…”

Section: Introductionmentioning

confidence: 99%

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Neonatal maternal separation opposes the facilitatory effect of castration on the respiratory response to hypercapnia of the adult male rat: Evidence for the involvement of the medial amygdala

Tenorio‐Lopes

Henry

Marques

et al. 2017

J Neuroendocrinology

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Respiratory manifestations of panic disorder (PD) include a greater respiratory instability and enhanced responsiveness to CO compared to normal individuals. Although the prevalence of PD is approximately three times greater in women compared to men, the origins of this sexual dimorphism remain poorly understood. Similar to PD patients, adult female rats previously subjected to neonatal maternal separation (NMS) show an increase in their ventilatory response to CO . Because this effect of NMS is not observed in males, we hypothesised that testosterone prevents NMS-induced hyper-responsiveness to CO . Pups subjected to NMS were placed in an incubator for 3 h d from postnatal days 3-12. Control pups remained undisturbed. At adulthood (8-10 weeks of age), rats were then subjected either to sham surgery or castration. Fourteen days later, breathing was measured at rest (room air) and during acute exposure to hypercapnia (5 and 10% CO for 10 minutes each) using plethysmography. To gain insight into the mechanisms involved, c-fos expression was used as an indicator of neuronal activation. Brains were collected following air or CO exposure for quantification of c-fos positive cells by immunohistochemistry in selected regions, including the paraventricular nucleus of the hypothalamus, the dorsomedial hypothalamus and the amygdalar complex. Castration produced a 100% increase of hyperventilatory response to 10% CO in control rats. Unexpectedly, castration had no effect on the hyperventilatory response of NMS rats. The intensity of the hypercapnic response was inversely correlated with c-fos expression in the medial amygdala. We conclude that testosterone prevents the hyper-responsiveness to CO , whereas NMS attenuates sensitivity to hormone withdrawal. We propose that an inhibitory influence from the medial amygdala contributes to this effect.

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Sex‐Specific Effects of Stress on Respiratory Control: Plasticity, Adaptation, and Dysfunction

Tenorio‐Lopes

Kinkead

2021

Comprehensive Physiology

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As our understanding of respiratory control evolves, we appreciate how the basic neurobiological principles of plasticity discovered in other systems shape the development and function of the respiratory control system. While breathing is a robust homeostatic function, there is growing evidence that stress disrupts respiratory control in ways that predispose to disease. Neonatal stress (in the form of maternal separation) affects "classical" respiratory control structures such as the peripheral O 2 sensors (carotid bodies) and the medulla (e.g., nucleus of the solitary tract). Furthermore, early life stress disrupts the paraventricular nucleus of the hypothalamus (PVH), a structure that has emerged as a primary determinant of the intensity of the ventilatory response to hypoxia. Although underestimated, the PVH's influence on respiratory function is a logical extension of the hypothalamic control of metabolic demand and supply. In this article, we review the functional and anatomical links between the stress neuroendocrine axis and the medullary network regulating breathing. We then present the persistent and sex-specific effects of neonatal stress on respiratory control in adult rats. The similarities between the respiratory phenotype of stressed rats and clinical manifestations of respiratory control disorders such as sleep-disordered breathing and panic attacks are remarkable. These observations are in line with the scientific consensus that the origins of adult disease are often found among developmental and biological disruptions occurring during early life. These observations bring a different perspective on the structural hierarchy of respiratory homeostasis and point to new directions in our understanding of the etiology of respiratory control disorders.

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A Neural Systems Approach to the Study of the Respiratory-Type Panic Disorder

Cited by 9 publications

References 429 publications

Amiloride modulation of carbon dioxide hypersensitivity and thermal nociceptive hypersensitivity induced by interference with early maternal environment

Amiloride modulation of carbon dioxide hypersensitivity and thermal nociceptive hypersensitivity induced by interference with early maternal environment

Neonatal maternal separation opposes the facilitatory effect of castration on the respiratory response to hypercapnia of the adult male rat: Evidence for the involvement of the medial amygdala

Sex‐Specific Effects of Stress on Respiratory Control: Plasticity, Adaptation, and Dysfunction

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