RTN TRH causes prolonged respiratory stimulation

Cream, Carlos; Li, Aihua; Nattie, Eugene E.

doi:10.1152/jappl.1997.83.3.792

Cited by 19 publications

(14 citation statements)

References 30 publications

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“…(Li and Nattie, 2002)). Injections of thyrotropin releasing hormone, a substance that activates the ccRTN neurons also activate both phrenic rate and amplitude (Cream et al, 1997) and injections of muscimol into the RTN region reduce breathing frequency in conscious rats, at least transiently (Nattie and Li, 2000). Yet, RTN acidification in conscious and in anesthetized rats stimulate breathing exclusively through an increase in tidal volume (Li and Nattie, 1997; Li et al, 1999).…”

Section: The Ccrtn Neurons Stimulate Inspiratory Motor Activitymentioning

confidence: 99%

Retrotrapezoid nucleus and parafacial respiratory group

Guyenet

Mulkey

2010

Respiratory Physiology & Neurobiology

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The rat retrotrapezoid nucleus (RTN) contains about 2000 Phox2b-expressing glutamatergic neurons (ccRTN neurons; 800 in mice) with a well-understood developmental lineage. ccRTN neuron development fails in mice carrying a Phox2b mutation commonly present in the congenital central hypoventilation syndrome. In adulthood, ccRTN neurons regulate the breathing rate and intensity, and may regulate active expiration along with other neighboring respiratory neurons. Prenatally, ccRTN neurons form an autonomous oscillator (embryonic parafacial group, e-pF) that activates and possibly paces inspiration. The pacemaker properties of the ccRTN neurons probably vanish after birth to be replaced by synaptic drives. The neonatal parafacial respiratory group (pfRG) may represent a transitional phase during which ccRTN neurons lose their group pacemaker properties. ccRTN neurons are activated by acidification via an intrinsic mechanism or via ATP released by glia. In summary, throughout life, ccRTN neurons seem to be a critical hub for the regulation of CO2 via breathing.

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Section: The Ccrtn Neurons Stimulate Inspiratory Motor Activitymentioning

confidence: 99%

Retrotrapezoid nucleus and parafacial respiratory group

Guyenet

Mulkey

2010

Respiratory Physiology & Neurobiology

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“…There are heavy projections from 5-HT neurons within the medullary raphé nuclei to the major respiratory nuclei, including hypoglossal and phrenic motor neurons (Holtman, Jr. et al, 1984a, 1984b; Connelly et al, 1989; Smith et al, 1989; Thor and Helke, 1989; Henry and Manaker, 1998; Aungst et al, 2008). Exogenous 5-HT, TRH and SP each stimulate respiratory motor output both in vivo and in vitro (Lalley, 1986; Morin et al, 1991; Monteau et al, 1994; Lalley et al, 1995; Hilaire et al, 1997; Cream et al, 1997, 1999; Pena and Ramirez, 2002, 2004; Manzke et al, 2003; Richerson, 2004; Brandes et al, 2006). Stimulation of raphé neurons causes an increase in respiratory output due to release of these transmitters (Lalley et al, 1986; Morin et al, 1990; Aungst et al, 2008), as recently reviewed in detail (Richerson, 2004; Hodges and Richerson, 2008b).…”

Section: Evidence That Serotonergic Neurons Are Respiratory Chemosmentioning

confidence: 99%

Medullary serotonin neurons and central CO2 chemoreception

Corcoran

Hodges

et al. 2009

Respiratory Physiology & Neurobiology

135

128

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Serotonergic (5-HT) neurons are putative central respiratory chemoreceptors, aiding in the brain's ability to detect arterial changes in P CO 2 and implement appropriate ventilatory responses to maintain blood homeostasis. These neurons are in close proximity to large medullary arteries and are intrinsically chemosensitive in vitro, characteristics expected for chemoreceptors. 5-HT neurons of the medullary raphé are stimulated by hypercapnia in vivo, and their disruption results in a blunted hypercapnic ventilatory response. More recently, data collected from transgenic and knock-out mice have provided further insight into the role of 5-HT in chemosensitivity. This review summarizes current evidence in support of the hypothesis that 5-HT neurons are central chemoreceptors, and addresses arguments made against this role. We also briefly explore the relationship between the medullary raphé and another chemoreceptive site, the retrotrapezoid nucleus, and discuss how they may interact during hypercapnia to produce a robust ventilatory response.

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“…There is a growing body of evidence that there is an association between TRH and the respiratory system. Injecting TRH into an important component of the rostral ventrolateral medulla, the retrotrapezoid nucleus, of anesthetized rats had powerful stimulatory effects on the product of integrated phrenic amplitude and frequency, and this response was dose-dependent 25. There was an increase in ventilation, O 2 consumption, and body temperature after TRH injection into the retrotrapezoid nucleus in conscious rats, and it was concluded that TRH could have an important role as a state-dependent modulator of breathing control 26.…”

Section: Discussionmentioning

confidence: 98%

End-tidal CO2 levels lower in subclinical and overt hypothyroidism than healthy controls; no relationship to thyroid function tests

Ansarin

Niroomand

Najafipour

et al. 2011

IJGM

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BackgroundHypoventilation is a frequently suspected complication of hypothyroidism.ObjectiveIn this study we examined the hypothesis that changes in alveolar ventilation, as measured by end-tidal carbon dioxide (Et-CO2), differ between patients with mild (subclinical) and overt (clinical) thyroid hormone deficiency, and both differ from healthy control subjects.MethodsA total of 95 subjects, including 33 with subclinical hypothyroidism (an elevated thyroid-stimulating hormone (TSH) level and a normal thyroxin (fT4) level), 31 with overt hypothyroidism (elevated TSH and decreased fT4), and 31 healthy controls. All subjects were female and were evaluated clinically by an endocrinologist for evidence of thyroid disease and categorized on the basis of thyroid hormone levels. Et-CO2 was measured using a capnograph. Et-CO2 levels were measured three times and the mean value was considered as the mean level for the individual.ResultsMean Et-CO2 values of the subclinical hypothyroidism group were significantly lower than those of the healthy controls (31.79 ± 2.75 vs 33.81 ± 2.38; P = 0.01). Moreover, mean Et-CO2 values for the overt hypothyroidism group were significantly lower than those for healthy controls (32.13 ± 3.07 vs 33.81 ± 2.38; P = 0.04). There was a significant correlation between Et-CO2 values and TSH levels (r = −0.24; P = 0.01). However, Et-CO2 values were not correlated with fT4 levels (r = 0.13; P = 0.20).ConclusionsAlveolar ventilation, as inferred from lower Et-CO2 levels, is higher in subjects with subclinical hypothyroidism and overt hypothyroidism (lower Et-CO2) than in healthy controls. Furthermore, Et-CO2 levels have no relationship to the levels of TSH or fT4. The lower Et-CO2 in these patients with hypothyroidism, particularly at the subclinical stage, suggests presence of hyperventilation, which may be related to direct effect of TRH on respiratory center or to local changes within the lung.

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RTN TRH causes prolonged respiratory stimulation

Cited by 19 publications

References 30 publications

Retrotrapezoid nucleus and parafacial respiratory group

Retrotrapezoid nucleus and parafacial respiratory group

Medullary serotonin neurons and central CO2 chemoreception

End-tidal CO2 levels lower in subclinical and overt hypothyroidism than healthy controls; no relationship to thyroid function tests

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