Lack of long term facilitation of ventilation after exposure to hypoxia in goats

Dwinell, Melinda R.; Janssen, P. L.; Bisgard, G. E.

doi:10.1016/s0034-5687(96)02522-4

Cited by 38 publications

(24 citation statements)

References 15 publications

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“…For example, HVD has been observed in awake humans (155,167,350,351), awake and anesthetized cats (405), awake rats (229,382), anesthetized rats, as a decline in phrenic nerve activity (156,375), and in anesthetized rabbits (136), but is not observed in awake dogs (44, 60). Perhaps more confounding, in awake goats some groups detect HVD (120,121,229,382), while others do not (2,76,285). Studies on awake rats that have not reported an occurrence of HVD (2) may be explained by the short time course of HVD (109), such that ventilation may have already stabilized at a lower level by the time steady state HVR measurements were made.…”

Section: Physiological and Molecular Responses To Brief Hypoxic Exposmentioning

confidence: 99%

“…However, other studies show that ventilatory LTF may be mediated by the sum of synaptic changes in genioglossal, hypoglossal, and intercostal motor responses, in addition to phrenic responses (103, 234, 243, 321). The hypoxic stimulus for LTF must be intermittent hypoxia as LTF is not induced by continuous hypoxia of the same duration as a bout of intermittent hypoxic episodes (e.g., 25 or 50 min) (76, 416). …”

Section: Physiological and Molecular Responses To Episodic Hypoxic Exmentioning

confidence: 99%

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Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis

Pamenter

Powell

2016

Comprehensive Physiology

104

101

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Ventilatory responses to hypoxia vary widely depending on the pattern and length of hypoxic exposure. Acute, prolonged, or intermittent hypoxic episodes can increase or decrease breathing for seconds to years, both during the hypoxic stimulus, and also after its removal. These myriad effects are the result of a complicated web of molecular interactions that underlie plasticity in the respiratory control reflex circuits and ultimately control the physiology of breathing in hypoxia. Since the time domains of the physiological hypoxic ventilatory response (HVR) were identified, considerable research effort has gone toward elucidating the underlying molecular mechanisms that mediate these varied responses. This research has begun to describe complicated and plastic interactions in the relay circuits between the peripheral chemoreceptors and the ventilatory control circuits within the central nervous system. Intriguingly, many of these molecular pathways seem to share key components between the different time domains, suggesting that varied physiological HVRs are the result of specific modifications to overlapping pathways. This review highlights what has been discovered regarding the cell and molecular level control of the time domains of the HVR, and highlights key areas where further research is required. Understanding the molecular control of ventilation in hypoxia has important implications for basic physiology and is emerging as an important component of several clinical fields.

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Section: Physiological and Molecular Responses To Brief Hypoxic Exposmentioning

confidence: 99%

Section: Physiological and Molecular Responses To Episodic Hypoxic Exmentioning

confidence: 99%

Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis

Pamenter

Powell

2016

Comprehensive Physiology

104

101

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“…1B). 12 Pattern sensitivity of respiratory plasticity was initially recognized in studies of ventilatory LTF (vLTF) in goats, 46,47 and subsequently observed in rat 48,49 and human vLTF. [50][51][52][53][54][55] Interestingly, vLTF in humans requires slightly elevated carbon dioxide (CO 2 ) during AIH.…”

Section: Pattern Sensitivitymentioning

confidence: 99%

Hypoxia‐induced phrenic long‐term facilitation: emergent properties

Devinney

Huxtable

Nichols

et al. 2013

Annals of the New York Academy of Sciences

122

114

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Just as in other neural systems, plasticity is a hallmark of the neural system controlling breathing. One spinal mechanism of respiratory plasticity is phrenic long-term facilitation (pLTF) following acute intermittent hypoxia. Although cellular mechanisms giving rise to pLTF occur within the phrenic motor nucleus, different signaling cascades elicit pLTF in different conditions. These cascades, referred to as “Q” and “S" pathways to phrenic motor facilitation (pMF), interact via cross-talk inhibition. Whereas the Q pathway dominates pLTF after mild to moderate hypoxic episodes, the S pathway dominates after severe hypoxic episodes. The biological significance of multiple pathways to pMF is not known. We discuss the possibility that interactions between pathways confer emergent properties to pLTF, including: 1) pattern sensitivity and 2) metaplasticity. Understanding these mechanisms and their interactions may enable us to optimize intermittent hypoxia induced plasticity as a treatment for patients that suffer from ventilatory impairment or other motor deficits.

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“…Probably the first description of LTF in the literature was the report of serotonin-dependent “afterdischarge” in phrenic activity in anesthetized cats in response to repeated bouts of carotid sinus nerve stimulation [14,15]. The hypoxic stimulus for LTF must be intermittent as it is not induced by continuous hypoxia of the same duration as the sum of the intermittent episodes [16]. …”

Section: Ltf – Historically a Serotonin-dependent Pathwaymentioning

confidence: 99%

Signalling mechanisms of long term facilitation of breathing with intermittent hypoxia

Pamenter

Powell

2013

F1000Prime Rep

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Intermittent hypoxia causes long-term facilitation (LTF) of respiratory motor nerve activity and ventilation, which manifests as a persistent increase over the normoxic baseline for an hour or more after the acute hypoxic ventilatory response. LTF is likely involved in sleep apnea, but its exact role is uncertain. Previously, LTF was defined as a serotonergic mechanism, but new evidence shows that multiple signaling pathways can elicit LTF. This raises new questions about the interactions between signaling pathways in different time domains of the hypoxic ventilatory response, which can no longer be defined simply in terms of neurochemical mechanisms.

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Lack of long term facilitation of ventilation after exposure to hypoxia in goats

Cited by 38 publications

References 15 publications

Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis

Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis

Hypoxia‐induced phrenic long‐term facilitation: emergent properties

Signalling mechanisms of long term facilitation of breathing with intermittent hypoxia

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