Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats
Autor(a) principal: | |
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Data de Publicação: | 2006 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/28847 http://dx.doi.org/10.1113/jphysiol.2005.103788 |
Resumo: | The rat retrotrapezoid nucleus (RTN) contains pH-sensitive neurons that are putative central chemoreceptors. Here, we examined whether these neurons respond to peripheral chemoreceptor stimulation and whether the input is direct from the solitary tract nucleus (NTS) or indirect via the respiratory network. A dense neuronal projection from commissural NTS (commNTS) to RTN was revealed using the anterograde tracer biotinylated dextran amine (BDA). Within RTN, 51% of BDA-labelled axonal varicosities contained detectable levels of vesicular glutamate transporter-2 (VGLUT2) but only 5% contained glutamic acid decarboxylase-67 (GAD67). Awake rats were exposed to hypoxia (n = 6) or normoxia (n = 5) 1 week after injection of the retrograde tracer cholera toxin B (CTB) into RTN. Hypoxia-activated neurons were identified by the presence of Fos-immunoreactive nuclei. CommNTS neurons immunoreactive for both Fos and CTB were found only in hypoxia-treated rats. VGLUT2 mRNA was detected in 92 +/- 13% of these neurons whereas only 12 +/- 9% contained GAD67 mRNA. in urethane-chloralose-anaesthetized rats, bilateral inhibition of the RTN with muscimol eliminated the phrenic nerve discharge (PND) at rest, during hyperoxic hypercapnia (10% CO2), and during peripheral chemoreceptor stimulation (hypoxia and/or i.v. sodium cyanide, NaCN). RTN CO2-activated neurons were recorded extracellularly in anaesthetized intact or vagotomized rats. These neurons were strongly activated by hypoxia (10-15% O-2; 30 s) or by NaCN. Hypoxia and NaCN were ineffective in rats with carotid chemoreceptor denervation. Bilateral injection of muscimol into the ventral respiratory column 1.5 mm caudal to RTN eliminated PND and the respiratory modulation of RTN neurons. Muscimol did not change the threshold and sensitivity of RTN neurons to hyperoxic hypercapnia nor their activation by peripheral chemoreceptor stimulation. in conclusion, RTN neurons respond to brain P-CO2 presumably via their intrinsic chemosensitivity and to carotid chemoreceptor activation via a direct glutamatergic pathway from commNTS that bypasses the respiratory network. RTN neurons probably contribute a portion of the chemical drive to breathe. |
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Takakura, Ana Carolina Thomaz [UNIFESP]Moreira, Thiago Santos [UNIFESP]Colombari, Eduardo [UNIFESP]West, Gavin H.Stornetta, Ruth L.Guyenet, Patrice G.Univ VirginiaUniversidade Federal de São Paulo (UNIFESP)2016-01-24T12:41:07Z2016-01-24T12:41:07Z2006-04-15Journal of Physiology-london. Oxford: Blackwell Publishing, v. 572, n. 2, p. 503-523, 2006.0022-3751http://repositorio.unifesp.br/handle/11600/28847http://dx.doi.org/10.1113/jphysiol.2005.10378810.1113/jphysiol.2005.103788WOS:000237225300017The rat retrotrapezoid nucleus (RTN) contains pH-sensitive neurons that are putative central chemoreceptors. Here, we examined whether these neurons respond to peripheral chemoreceptor stimulation and whether the input is direct from the solitary tract nucleus (NTS) or indirect via the respiratory network. A dense neuronal projection from commissural NTS (commNTS) to RTN was revealed using the anterograde tracer biotinylated dextran amine (BDA). Within RTN, 51% of BDA-labelled axonal varicosities contained detectable levels of vesicular glutamate transporter-2 (VGLUT2) but only 5% contained glutamic acid decarboxylase-67 (GAD67). Awake rats were exposed to hypoxia (n = 6) or normoxia (n = 5) 1 week after injection of the retrograde tracer cholera toxin B (CTB) into RTN. Hypoxia-activated neurons were identified by the presence of Fos-immunoreactive nuclei. CommNTS neurons immunoreactive for both Fos and CTB were found only in hypoxia-treated rats. VGLUT2 mRNA was detected in 92 +/- 13% of these neurons whereas only 12 +/- 9% contained GAD67 mRNA. in urethane-chloralose-anaesthetized rats, bilateral inhibition of the RTN with muscimol eliminated the phrenic nerve discharge (PND) at rest, during hyperoxic hypercapnia (10% CO2), and during peripheral chemoreceptor stimulation (hypoxia and/or i.v. sodium cyanide, NaCN). RTN CO2-activated neurons were recorded extracellularly in anaesthetized intact or vagotomized rats. These neurons were strongly activated by hypoxia (10-15% O-2; 30 s) or by NaCN. Hypoxia and NaCN were ineffective in rats with carotid chemoreceptor denervation. Bilateral injection of muscimol into the ventral respiratory column 1.5 mm caudal to RTN eliminated PND and the respiratory modulation of RTN neurons. Muscimol did not change the threshold and sensitivity of RTN neurons to hyperoxic hypercapnia nor their activation by peripheral chemoreceptor stimulation. in conclusion, RTN neurons respond to brain P-CO2 presumably via their intrinsic chemosensitivity and to carotid chemoreceptor activation via a direct glutamatergic pathway from commNTS that bypasses the respiratory network. RTN neurons probably contribute a portion of the chemical drive to breathe.Univ Virginia, Hlth Syst, Dept Pharmacol, Charlottesville, VA 22908 USAUNIFESP, EPM, Dept Physiol, BR-04023060 São Paulo, SP, BrazilUNIFESP, EPM, Dept Physiol, BR-04023060 São Paulo, SP, BrazilWeb of Science503-523engBlackwell PublishingJournal of Physiology-londonPeripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/288472021-09-30 17:26:14.164metadata only accessoai:repositorio.unifesp.br:11600/28847Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:22:28.836715Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats |
title |
Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats |
spellingShingle |
Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats Takakura, Ana Carolina Thomaz [UNIFESP] |
title_short |
Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats |
title_full |
Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats |
title_fullStr |
Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats |
title_full_unstemmed |
Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats |
title_sort |
Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats |
author |
Takakura, Ana Carolina Thomaz [UNIFESP] |
author_facet |
Takakura, Ana Carolina Thomaz [UNIFESP] Moreira, Thiago Santos [UNIFESP] Colombari, Eduardo [UNIFESP] West, Gavin H. Stornetta, Ruth L. Guyenet, Patrice G. |
author_role |
author |
author2 |
Moreira, Thiago Santos [UNIFESP] Colombari, Eduardo [UNIFESP] West, Gavin H. Stornetta, Ruth L. Guyenet, Patrice G. |
author2_role |
author author author author author |
dc.contributor.institution.none.fl_str_mv |
Univ Virginia Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Takakura, Ana Carolina Thomaz [UNIFESP] Moreira, Thiago Santos [UNIFESP] Colombari, Eduardo [UNIFESP] West, Gavin H. Stornetta, Ruth L. Guyenet, Patrice G. |
description |
The rat retrotrapezoid nucleus (RTN) contains pH-sensitive neurons that are putative central chemoreceptors. Here, we examined whether these neurons respond to peripheral chemoreceptor stimulation and whether the input is direct from the solitary tract nucleus (NTS) or indirect via the respiratory network. A dense neuronal projection from commissural NTS (commNTS) to RTN was revealed using the anterograde tracer biotinylated dextran amine (BDA). Within RTN, 51% of BDA-labelled axonal varicosities contained detectable levels of vesicular glutamate transporter-2 (VGLUT2) but only 5% contained glutamic acid decarboxylase-67 (GAD67). Awake rats were exposed to hypoxia (n = 6) or normoxia (n = 5) 1 week after injection of the retrograde tracer cholera toxin B (CTB) into RTN. Hypoxia-activated neurons were identified by the presence of Fos-immunoreactive nuclei. CommNTS neurons immunoreactive for both Fos and CTB were found only in hypoxia-treated rats. VGLUT2 mRNA was detected in 92 +/- 13% of these neurons whereas only 12 +/- 9% contained GAD67 mRNA. in urethane-chloralose-anaesthetized rats, bilateral inhibition of the RTN with muscimol eliminated the phrenic nerve discharge (PND) at rest, during hyperoxic hypercapnia (10% CO2), and during peripheral chemoreceptor stimulation (hypoxia and/or i.v. sodium cyanide, NaCN). RTN CO2-activated neurons were recorded extracellularly in anaesthetized intact or vagotomized rats. These neurons were strongly activated by hypoxia (10-15% O-2; 30 s) or by NaCN. Hypoxia and NaCN were ineffective in rats with carotid chemoreceptor denervation. Bilateral injection of muscimol into the ventral respiratory column 1.5 mm caudal to RTN eliminated PND and the respiratory modulation of RTN neurons. Muscimol did not change the threshold and sensitivity of RTN neurons to hyperoxic hypercapnia nor their activation by peripheral chemoreceptor stimulation. in conclusion, RTN neurons respond to brain P-CO2 presumably via their intrinsic chemosensitivity and to carotid chemoreceptor activation via a direct glutamatergic pathway from commNTS that bypasses the respiratory network. RTN neurons probably contribute a portion of the chemical drive to breathe. |
publishDate |
2006 |
dc.date.issued.fl_str_mv |
2006-04-15 |
dc.date.accessioned.fl_str_mv |
2016-01-24T12:41:07Z |
dc.date.available.fl_str_mv |
2016-01-24T12:41:07Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Journal of Physiology-london. Oxford: Blackwell Publishing, v. 572, n. 2, p. 503-523, 2006. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/28847 http://dx.doi.org/10.1113/jphysiol.2005.103788 |
dc.identifier.issn.none.fl_str_mv |
0022-3751 |
dc.identifier.doi.none.fl_str_mv |
10.1113/jphysiol.2005.103788 |
dc.identifier.wos.none.fl_str_mv |
WOS:000237225300017 |
identifier_str_mv |
Journal of Physiology-london. Oxford: Blackwell Publishing, v. 572, n. 2, p. 503-523, 2006. 0022-3751 10.1113/jphysiol.2005.103788 WOS:000237225300017 |
url |
http://repositorio.unifesp.br/handle/11600/28847 http://dx.doi.org/10.1113/jphysiol.2005.103788 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
Journal of Physiology-london |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
503-523 |
dc.publisher.none.fl_str_mv |
Blackwell Publishing |
publisher.none.fl_str_mv |
Blackwell Publishing |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1783460282911162368 |