A single minute lesion around the ventral respiratory group in medulla produces fatal apnea in cats

Hsieh, Jui-Hsiang; Chang, Ya‐Jen; Su, Chin Cheng; Hwang, Jaulang; Yen, Chen‐Tung; Chai, C. Y.

doi:10.1016/s0165-1838(98)00117-9

Cited by 18 publications

(15 citation statements)

References 28 publications

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“…However, as Ramirez et al (1998) also found, this apnoea was induced in only a limited proportion of animals following injections into seemingly identical regions. In the anaesthetized animals studied by Ramirez et al (1998) and Hsieh et al (1998), eupnoea never returned following injections of tetrotoxin or kainic acid, respectively, into the pre‐Bötzinger complex. In the present study, eupnoea returned transiently or permanently following activation of the carotid chemoreceptors by injections of sodium cyanide.…”

Section: Discussionmentioning

confidence: 90%

Transient, reversible apnoea following ablation of the pre‐Bötzinger complex in rats

St-Jacques

St‐John

1999

The Journal of Physiology

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The rhythmic alterations of cranial and spinal nerves which are characteristic of eupnoeic ventilatory activity are dependent upon two interrelated processes. Neuronal mechanisms within the pontile and medullary brainstem are responsible for generating the eupnoeic rhythm. For this rhythm to be expressed in activities of cranial and spinal nerves, a level of tonic neuronal input is required (e.g. Euler, 1986;St-John, 1998a). Thus, eupnoea could be eliminated following ablation of neurons which are responsible for its neurogenesis andÏor which provide for a tonic input. The necessity of a tonic input for eupnoea to be manifested is inherent in the concept of an 'apnoeic threshold' for arterial partial pressures of carbon dioxide. Hence, apnoea can be induced by hyperventilation of anaesthetized or decerebrate preparations (see Cherniack et al. 1979;Euler, 1986 for discussion). The apnoea which follows a blockade of neuronal activities in extensive regions on or near the ventrolateral medullary surface is likewise considered to result from the elimination of a tonic input (see St-John, 1998a for review). As opposed to a tonic input, neuronal activities within a rostral medullary pre-B otzinger complex have been hypothesized to be an exclusive mechanism for generating the eupnoeic rhythm (Smith et al. 1990(Smith et al. , 1991Rekling & Feldman, 1998). This hypothesis was based upon the finding that ablation of neurons in this region eliminates the rhythmic activity of an in vitro brainstem-spinal cord preparation of the neonatal rat. Yet, this rhythmic activity differs markedly from eupnoea in vivo but appears identical with gasping (St-John, 1996;1998a). Ablation of the pre-B otzinger complex in vivo has led to inconsistent findings. In anaesthetized or decerebrate adult cats, eupnoea continued following the placement of multiple lesions which, in sum, destroyed the entire pre-B otzinger complex (Speck & Feldman, 1982;Speck & Beck, 1989). In decerebrate newborn rats, unilateral injections of the neurotoxin kainic acid into the pre-B otzinger complex did not eliminate eupnoea (Huang et al. 1997). In anaesthetized adult rats, apnoea is reported following bilateral injections of the GABA agonist muscimol into the rostral ventrolateral medulla (Koshiya et al. 1993;Koshiya & Guyenet, 1996). Recently, Ramirez et al. 1998 reported that injections of reversible blockers of synaptic activity into the pre-B otzinger complex of anaesthetized adult cats caused transient reductions of phrenic activity. At some, but not all of these effective sites, bilateral injections of

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Section: Discussionmentioning

confidence: 90%

Transient, reversible apnoea following ablation of the pre‐Bötzinger complex in rats

St-Jacques

St‐John

1999

The Journal of Physiology

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“…In rabbit and rat, splitting the medulla oblongata in the midline simply allows the two hemidiaphragms to contract independently (Peever et al, 1998). In human and cat, splitting the medulla oblongata in the midline causes apnea (Hsieh et al, 1998;Bogousslavsky et al, 1990;Gromysz and Karczewski, 1982) unless the hypercarbic stimulus is large (Gromysz and Karczewski, 1982). Such findings suggest that the ensemble of rhythm-generating neurons have a physiological threshold for generation of an integrated output that is then passed to premotor neurons in order to generate a normal respiratory activity; and that this threshold differs in different species.…”

Section: Physiology Of Different Parts Of the Raphementioning

confidence: 99%

Peptides, Serotonin, and Breathing

Pilowsky

2014

Progress in Brain Research

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“… 15–17 Second, brain stem rhythmic respiratory output is eliminated when the PreBötC is ablated 12,18,19 . Finally, perturbations of neuronal function in and around the PreBötC severely disrupt breathing in mammals 18,20 . The respiratory rhythm results from a dynamic coupling between both synaptic and intrinsic membrane properties, including those of pacemaker neurons in the PreBötC 21–26 (Fig.…”

Section: Generation Of Respiratory Rhythmmentioning

confidence: 99%

Neuronal network properties underlying the generation of gasping

Peña

2009

Clin Exp Pharma Physio

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1. The pre-Bötzinger complex (PreBötC) generates different inspiratory rhythms. Under control normoxic conditions, a mixture of intrinsic and synaptic properties underlies the generation of eupnoea by the PreBötC. Under hypoxia, those network properties change and modify the respiratory rhythm pattern. Hypoxia can be caused by a reduction in oxygen availability in the environment, inadequate oxygen transport, an inability of tissues to use oxygen or several pathological conditions. 2. During severe hypoxia, the network properties within the PreBötC are reconfigured whereby the network no longer generates eupnoea, but instead generates a new rhythm, named gasping. Such reconfiguration includes changes in synaptic and intrinsic properties triggered by hypoxia itself, as well as the influence of different neuromodulators released during hypoxia. Gasping has been considered an important arousal mechanism that triggers autoresuscitation. Dysregulation of gasping has been proposed to result in failure to autoresuscitate and has been hypothesised to contribute to Sudden Infant Death Syndrome. 3. Precisely which synaptic and/or neuronal intrinsic membrane properties are critical to central respiratory rhythmogenesis, in either normoxia or hypoxia, is still the subject of considerable debate. In the present article I review how hypoxia alters the respiratory network and discuss my hypotheses regarding the cellular and network mechanisms involved in gasping rhythm generation. Finally, I review changes in the hypoxic response during postnatal development and the contribution of several neuromodulators to such a response.

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A single minute lesion around the ventral respiratory group in medulla produces fatal apnea in cats

Cited by 18 publications

References 28 publications

Transient, reversible apnoea following ablation of the pre‐Bötzinger complex in rats

Transient, reversible apnoea following ablation of the pre‐Bötzinger complex in rats

Peptides, Serotonin, and Breathing

Neuronal network properties underlying the generation of gasping

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