Evidence of a suffocation alarm system within the periaqueductal gray matter of the rat

Schimitel, Fagna Giacomin; Almeida, Gustavo Maia de; Pitol, D.N.; Armini, R.S.; Tufik, Sérgio; Schenberg, Luiz Carlos

doi:10.1016/j.neuroscience.2011.10.032

Cited by 74 publications

(85 citation statements)

References 103 publications

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“…Some authors have proposed that dPAG stimulation induces autonomic and behavioral responses similar to the symptoms of panic attacks; thus, this area may be involved in the origin of panic disorder [25,35,36,44,50,66]. Recently, Schimitel et al [67] suggested that activation of suffocation alarm system in the PAG precipitates panic attacks and potentiates the subject behavioral responses to hypercapnia. The results of our study add to this scenario that dPAG is also important for ventilatory response to hypercapnia because dlPAG/ dmPAG lesions reduced the CO 2 -drive to breathe.…”

Section: Discussionmentioning

confidence: 99%

Periaqueductal gray matter modulates the hypercapnic ventilatory response

Tenorio‐Lopes

Patrone

Bícego

et al. 2012

Pflugers Arch - Eur J Physiol

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The periaqueductal gray (PAG) is a midbrain structure directly involved in the modulation of defensive behaviors. It has direct projections to several central nuclei that are involved in cardiorespiratory control. Although PAG stimulation is known to elicit respiratory responses, the role of the PAG in the CO(2)-drive to breathe is still unknown. The present study assessed the effect of chemical lesion of the dorsolateral and dorsomedial and ventrolateral/lateral PAG (dlPAG, dmPAG, and vPAG, respectively) on cardiorespiratory and thermal responses to hypercapnia. Ibotenic acid (IBO) or vehicle (PBS, Sham group) was injected into the dlPAG, dmPAG, or vPAG of male Wistar rats. Rats with lesions outside the dlPAG, dmPAG, or vPAG were considered as negative controls (NC). Pulmonary ventilation (VE: ), mean arterial pressure (MAP), heart rate (HR), and body temperature (Tb) were measured in unanesthetized rats during normocapnia and hypercapnic exposure (5, 15, 30 min, 7 % CO(2)). IBO lesioning of the dlPAG/dmPAG caused 31 % and 26.5 % reductions of the respiratory response to CO(2) (1,094.3 ± 115 mL/kg/min) compared with Sham (1,589.5 ± 88.1 mL/kg/min) and NC groups (1,488.2 ± 47.7 mL/kg/min), respectively. IBO lesioning of the vPAG caused 26.6 % and 21 % reductions of CO(2) hyperpnea (1,215.3 ± 108.6 mL/kg/min) compared with Sham (1,657.3 ± 173.9 mL/kg/min) and NC groups (1,537.6 ± 59.3). Basal VE: , MAP, HR, and Tb were not affected by dlPAG, dmPAG, or vPAG lesioning. The results suggest that dlPAG, dmPAG, and vPAG modulate hypercapnic ventilatory responses in rats but do not affect MAP, HR, or Tb regulation in resting conditions or during hypercapnia.

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Section: Discussionmentioning

confidence: 99%

Periaqueductal gray matter modulates the hypercapnic ventilatory response

Tenorio‐Lopes

Patrone

Bícego

et al. 2012

Pflugers Arch - Eur J Physiol

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“…As mentioned above, the dorsal PAG is related to panic responses and is also responsive to life threatening events, including cardiac pain (Albutaihi et al, 2004), interoceptive signals of hypoxia (Berquin et al, 2000;Schimitel et al, 2012), inhalation of hypercarbic gas (Johnson et al, 2011), and predator threats (Canteras and Goto, 1999;Dielenberg et al, 2001). Importantly, the dorsal PAG has been shown to support fear learning.…”

Section: Pag and Fear Learningmentioning

confidence: 97%

The periaqueductal gray and primal emotional processing critical to influence complex defensive responses, fear learning and reward seeking

Motta

Carobrez

Canteras

2017

Neuroscience & Biobehavioral Reviews

119

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“…Obstructions to respiration invoke intense innate responses across animal species (Schimitel et al 2012). The brain is thought to detect suffocation through sensors of blood O 2 and CO 2 partial pressure located in the carotid body (Finley and Katz 1992 from the carotid are processed by the nucleus of the solitary tract (NTS) that, in turn, targets respiration nuclei in the medulla for respiratory adaptations (Loewy and Burton 1978;Paton et al 2001), as well as higher structures involved in the generation of defensive responses such as PAG, CEA, and the paraventricular nucleus of the hypothalamus (Ricardo and Tongju Koh 1978).…”

Section: Suffocation Signalsmentioning

confidence: 99%

“…The brain is thought to detect suffocation through sensors of blood O 2 and CO 2 partial pressure located in the carotid body (Finley and Katz 1992 from the carotid are processed by the nucleus of the solitary tract (NTS) that, in turn, targets respiration nuclei in the medulla for respiratory adaptations (Loewy and Burton 1978;Paton et al 2001), as well as higher structures involved in the generation of defensive responses such as PAG, CEA, and the paraventricular nucleus of the hypothalamus (Ricardo and Tongju Koh 1978). Indeed, severe hypoxia induces significant increases in c-Fos protein expression in the NTS and in the dorsolateral and lateral columns of the PAG (Casanova et al 2013), and lesions in the PAG suppress hypoxia-induced defensive behaviors (Schimitel et al 2012). Moreover, slice electrophysiology experiments have shown that the PAGd harbors hypoxia-responding neurons (Kramer et al 1999).…”

Section: Suffocation Signalsmentioning

confidence: 99%

The neural circuits of innate fear: detection, integration, action, and memorization

2016

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How fear is represented in the brain has generated a lot of research attention, not only because fear increases the chances for survival when appropriately expressed but also because it can lead to anxiety and stress-related disorders when inadequately processed. In this review, we summarize recent progress in the understanding of the neural circuits processing innate fear in rodents. We propose that these circuits are contained within three main functional units in the brain: a detection unit, responsible for gathering sensory information signaling the presence of a threat; an integration unit, responsible for incorporating the various sensory information and recruiting downstream effectors; and an output unit, in charge of initiating appropriate bodily and behavioral responses to the threatful stimulus. In parallel, the experience of innate fear also instructs a learning process leading to the memorization of the fearful event. Interestingly, while the detection, integration, and output units processing acute fear responses to different threats tend to be harbored in distinct brain circuits, memory encoding of these threats seems to rely on a shared learning system.

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Evidence of a suffocation alarm system within the periaqueductal gray matter of the rat

Cited by 74 publications

References 103 publications

Periaqueductal gray matter modulates the hypercapnic ventilatory response

Periaqueductal gray matter modulates the hypercapnic ventilatory response

The periaqueductal gray and primal emotional processing critical to influence complex defensive responses, fear learning and reward seeking

The neural circuits of innate fear: detection, integration, action, and memorization

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