Serotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanism
Autor(a) principal: | |
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Data de Publicação: | 2007 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/30218 http://dx.doi.org/10.1523/JNEUROSCI.4167-07.2007 |
Resumo: | Serotonin activates respiration and enhances the stimulatory effect of CO2 on breathing. the present study tests whether the mechanism involves the retrotrapezoid nucleus (RTN), a group of medullary glutamatergic neurons activated by extracellular brain pH and presumed to regulate breathing. We show that the RTN is innervated by both medullary and pontine raphe and receives inputs from thyrotropin-releasing hormone (TRH) and substance P-expressing neurons. Coexistence of serotonin and substance P in terminals within RTN confirmed that lower medullary serotonergic neurons innervate RTN. in vivo, unilateral injection of serotonin into RTN stimulated inspiratory motor activity, and pH-sensitive RTN neurons were activated by iontophoretic application of serotonin or substance P. in brain slices, pH-sensitive RTN neurons were activated by serotonin, substance P, and TRH. the effect of serotonin in slices was ketanserin sensitive and persisted in the presence of glutamate, GABA, glycine, and purinergic ionotropic receptor antagonists. Serotonin and pH had approximately additive effects on the discharge rate of RTN neurons, both in slices and in vivo. in slices, serotonin produced an inward current with little effect on conductance and had no effect on the pH-induced current. We conclude that (1) RTN receives input from multiple raphe nuclei, (2) serotonin, substance P, and TRH activate RTN chemoreceptors, and (3) excitatory effects of serotonin and pH are mediated by distinct ionic conductances. Thus, RTN neurons presumably contribute to the respiratory stimulation caused by serotonergic neurons, but serotonin seems without effect on the cellular mechanism by which RTN neurons detect pH. |
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Mulkey, Daniel K.Rosin, Diane L.West, GavinTakakura, Ana C. [UNIFESP]Moreira, Thiago S. [UNIFESP]Bayliss, Douglas A.Guyenet, Patrice G.Univ VirginiaUniversidade Federal de São Paulo (UNIFESP)2016-01-24T13:49:17Z2016-01-24T13:49:17Z2007-12-19Journal of Neuroscience. Washington: Soc Neuroscience, v. 27, n. 51, p. 14128-14138, 2007.0270-6474http://repositorio.unifesp.br/handle/11600/30218http://dx.doi.org/10.1523/JNEUROSCI.4167-07.200710.1523/JNEUROSCI.4167-07.2007WOS:000251910800025Serotonin activates respiration and enhances the stimulatory effect of CO2 on breathing. the present study tests whether the mechanism involves the retrotrapezoid nucleus (RTN), a group of medullary glutamatergic neurons activated by extracellular brain pH and presumed to regulate breathing. We show that the RTN is innervated by both medullary and pontine raphe and receives inputs from thyrotropin-releasing hormone (TRH) and substance P-expressing neurons. Coexistence of serotonin and substance P in terminals within RTN confirmed that lower medullary serotonergic neurons innervate RTN. in vivo, unilateral injection of serotonin into RTN stimulated inspiratory motor activity, and pH-sensitive RTN neurons were activated by iontophoretic application of serotonin or substance P. in brain slices, pH-sensitive RTN neurons were activated by serotonin, substance P, and TRH. the effect of serotonin in slices was ketanserin sensitive and persisted in the presence of glutamate, GABA, glycine, and purinergic ionotropic receptor antagonists. Serotonin and pH had approximately additive effects on the discharge rate of RTN neurons, both in slices and in vivo. in slices, serotonin produced an inward current with little effect on conductance and had no effect on the pH-induced current. We conclude that (1) RTN receives input from multiple raphe nuclei, (2) serotonin, substance P, and TRH activate RTN chemoreceptors, and (3) excitatory effects of serotonin and pH are mediated by distinct ionic conductances. Thus, RTN neurons presumably contribute to the respiratory stimulation caused by serotonergic neurons, but serotonin seems without effect on the cellular mechanism by which RTN neurons detect pH.Univ Virginia, Dept Pharmacol, Charlottesville, VA 22908 USAUniversidade Federal de São Paulo, Dept Physiol, Escola Paulista Med, BR-04023060 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Physiol, Escola Paulista Med, BR-04023060 São Paulo, BrazilWeb of Science14128-14138engSoc NeuroscienceJournal of Neurosciencechemosensitivityraphecentral respiratory controlventral medullary surfacepH signalingbrain sliceSerotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanisminfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/302182022-09-27 09:59:57.3metadata only accessoai:repositorio.unifesp.br:11600/30218Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-09-27T12:59:57Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Serotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanism |
title |
Serotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanism |
spellingShingle |
Serotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanism Mulkey, Daniel K. chemosensitivity raphe central respiratory control ventral medullary surface pH signaling brain slice |
title_short |
Serotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanism |
title_full |
Serotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanism |
title_fullStr |
Serotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanism |
title_full_unstemmed |
Serotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanism |
title_sort |
Serotonergic neurons activate chemosensitive retrotrapezoid nucleus neurons by a pH-independent mechanism |
author |
Mulkey, Daniel K. |
author_facet |
Mulkey, Daniel K. Rosin, Diane L. West, Gavin Takakura, Ana C. [UNIFESP] Moreira, Thiago S. [UNIFESP] Bayliss, Douglas A. Guyenet, Patrice G. |
author_role |
author |
author2 |
Rosin, Diane L. West, Gavin Takakura, Ana C. [UNIFESP] Moreira, Thiago S. [UNIFESP] Bayliss, Douglas A. Guyenet, Patrice G. |
author2_role |
author 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 |
Mulkey, Daniel K. Rosin, Diane L. West, Gavin Takakura, Ana C. [UNIFESP] Moreira, Thiago S. [UNIFESP] Bayliss, Douglas A. Guyenet, Patrice G. |
dc.subject.eng.fl_str_mv |
chemosensitivity raphe central respiratory control ventral medullary surface pH signaling brain slice |
topic |
chemosensitivity raphe central respiratory control ventral medullary surface pH signaling brain slice |
description |
Serotonin activates respiration and enhances the stimulatory effect of CO2 on breathing. the present study tests whether the mechanism involves the retrotrapezoid nucleus (RTN), a group of medullary glutamatergic neurons activated by extracellular brain pH and presumed to regulate breathing. We show that the RTN is innervated by both medullary and pontine raphe and receives inputs from thyrotropin-releasing hormone (TRH) and substance P-expressing neurons. Coexistence of serotonin and substance P in terminals within RTN confirmed that lower medullary serotonergic neurons innervate RTN. in vivo, unilateral injection of serotonin into RTN stimulated inspiratory motor activity, and pH-sensitive RTN neurons were activated by iontophoretic application of serotonin or substance P. in brain slices, pH-sensitive RTN neurons were activated by serotonin, substance P, and TRH. the effect of serotonin in slices was ketanserin sensitive and persisted in the presence of glutamate, GABA, glycine, and purinergic ionotropic receptor antagonists. Serotonin and pH had approximately additive effects on the discharge rate of RTN neurons, both in slices and in vivo. in slices, serotonin produced an inward current with little effect on conductance and had no effect on the pH-induced current. We conclude that (1) RTN receives input from multiple raphe nuclei, (2) serotonin, substance P, and TRH activate RTN chemoreceptors, and (3) excitatory effects of serotonin and pH are mediated by distinct ionic conductances. Thus, RTN neurons presumably contribute to the respiratory stimulation caused by serotonergic neurons, but serotonin seems without effect on the cellular mechanism by which RTN neurons detect pH. |
publishDate |
2007 |
dc.date.issued.fl_str_mv |
2007-12-19 |
dc.date.accessioned.fl_str_mv |
2016-01-24T13:49:17Z |
dc.date.available.fl_str_mv |
2016-01-24T13:49:17Z |
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 Neuroscience. Washington: Soc Neuroscience, v. 27, n. 51, p. 14128-14138, 2007. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/30218 http://dx.doi.org/10.1523/JNEUROSCI.4167-07.2007 |
dc.identifier.issn.none.fl_str_mv |
0270-6474 |
dc.identifier.doi.none.fl_str_mv |
10.1523/JNEUROSCI.4167-07.2007 |
dc.identifier.wos.none.fl_str_mv |
WOS:000251910800025 |
identifier_str_mv |
Journal of Neuroscience. Washington: Soc Neuroscience, v. 27, n. 51, p. 14128-14138, 2007. 0270-6474 10.1523/JNEUROSCI.4167-07.2007 WOS:000251910800025 |
url |
http://repositorio.unifesp.br/handle/11600/30218 http://dx.doi.org/10.1523/JNEUROSCI.4167-07.2007 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
Journal of Neuroscience |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
14128-14138 |
dc.publisher.none.fl_str_mv |
Soc Neuroscience |
publisher.none.fl_str_mv |
Soc Neuroscience |
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_ |
1802764165106892800 |