Controle inibitório do padrão de expiração ativa em ratos

Detalhes bibliográficos
Autor(a) principal: Flor, Karine Correa
Data de Publicação: 2018
Tipo de documento: Dissertação
Idioma: por
Título da fonte: Repositório Institucional da UFSCAR
Texto Completo: https://repositorio.ufscar.br/handle/ufscar/9951
Resumo: Late-expiratory neurons (late-E) located in the parafacial respiratory group (pFRG), a critical region for the emergence of active expiratory pattern, are conditional and remain silent at baseline conditions. In situations of metabolic challenges, these neurons become active and contribute to increase the abdominal motor activity during the late expiratory phase. It was found that late-E neurons are silent at rest due to inhibitory inputs. Interestingly, in conditions of sustained hypoxia (SH), commonly observed in people moving to high altitudes, this inhibitory drive is reduced and generates the active expiratory pattern. In the present study we hypothesized that the Bötzinger complex (BötC), located in the ventral respiratory column, plays an important inhibitory role on the emergence of active expiration. We also explored the possibility that BötC inhibitory mechanism is reduced after SH and the activation of this mechanism is able to normalize the expiratory pattern of SH rats. The aim of the present study was to explore the contribution of the BötC neurons in the generation of the active expiratory pattern in control and SH (10% O2, 24 h) rats. To reach this goal, we recorded the pulmonary ventilation (in vivo) and respiratory motor activity in in situ preparations of juvenile rats (60-80 g) to evaluate, under normocapnic and hypercapnic (8-10% CO2) conditions: i) activity patterns of BötC post-I (n=5) and aug-E (n=9) neurons of control rats; ii) changes in the respiratory pattern after BötC pharmacological disinhibition of control rats with gabazine (GABAA receptor antagonist, 250 μM, n=7) or strychnine (glycine receptor antagonist, 10 μM, n=7); iii) the respiratory pattern of SH rats in situ (n=7) and in vivo (n=12); iv) effects on the respiratory motor activity of control (n=7) and SH rats (n=7) after microinjections of L-glutamate in BötC (10 mM); v) changes in respiratory pattern of SH rats (n=8) promoted by the pharmacological disinhibition of the BötC with strychnine (10 μM). In control rats, post-I and aug-E neurons were recorded under hypercapnia (8% CO2). Hypercapnia evoked late-E activity in the abdominal nerve (AbN), in association with a decreased post-I activity and augmented aug-E activity. Regarding to the bilateral microinjections of gabazine in the BötC of control rats, we observed a decrease in baseline phrenic nerve (PN) bursts frequency and increases in the expiratory time and in the AbN activity, with the emergence of late-E bursts. On the other hand, bilateral microinjections of strychnine in the BötC of control rats diminished the PN, vagus (cVN) and AbN nerve amplitudes, but did not modify the 3-phase respiratory pattern; and attenuated the emergence of the active expiratory pattern under hypercapnia conditions. Concerning the basal ventilatory pattern of unanesthetized SH rats, we observed an increase in minute ventilation, associated with a higher respiratory frequency and tidal volume. These findings obtained in in vivo parallel with our data from in situ preparations, showing that SH evoked active expiratory pattern at baseline conditions. BötC stimulation of SH rats with L-glutamate was able to briefly abolish AbN late-E activity. In addition, BötC disinhibition of SH animals with strychnine eliminated the late-E AbN firing and restored the respiratory motor pattern, similarly to control animals. Taken together, our results indicate that BötC perform a relevant inhibitory role on the mechanisms of active expiratory pattern generation. In addition, short-term SH seems to change the activity of BötC neurons, reducing this inhibitory drive and contributing to the emergence late-E AbN activity at resting conditions in these animals.
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spelling Flor, Karine CorreaZoccal, Daniel Breseghellohttp://lattes.cnpq.br/1958567557189244http://lattes.cnpq.br/29880635991232564fde01e8-ca53-423c-910d-79a5c46a301c2018-05-10T14:20:39Z2018-05-10T14:20:39Z2018-02-22FLOR, Karine Correa. Controle inibitório do padrão de expiração ativa em ratos. 2018. Dissertação (Mestrado em Ciências Fisiológicas) – Universidade Federal de São Carlos, São Carlos, 2018. Disponível em: https://repositorio.ufscar.br/handle/ufscar/9951.https://repositorio.ufscar.br/handle/ufscar/9951Late-expiratory neurons (late-E) located in the parafacial respiratory group (pFRG), a critical region for the emergence of active expiratory pattern, are conditional and remain silent at baseline conditions. In situations of metabolic challenges, these neurons become active and contribute to increase the abdominal motor activity during the late expiratory phase. It was found that late-E neurons are silent at rest due to inhibitory inputs. Interestingly, in conditions of sustained hypoxia (SH), commonly observed in people moving to high altitudes, this inhibitory drive is reduced and generates the active expiratory pattern. In the present study we hypothesized that the Bötzinger complex (BötC), located in the ventral respiratory column, plays an important inhibitory role on the emergence of active expiration. We also explored the possibility that BötC inhibitory mechanism is reduced after SH and the activation of this mechanism is able to normalize the expiratory pattern of SH rats. The aim of the present study was to explore the contribution of the BötC neurons in the generation of the active expiratory pattern in control and SH (10% O2, 24 h) rats. To reach this goal, we recorded the pulmonary ventilation (in vivo) and respiratory motor activity in in situ preparations of juvenile rats (60-80 g) to evaluate, under normocapnic and hypercapnic (8-10% CO2) conditions: i) activity patterns of BötC post-I (n=5) and aug-E (n=9) neurons of control rats; ii) changes in the respiratory pattern after BötC pharmacological disinhibition of control rats with gabazine (GABAA receptor antagonist, 250 μM, n=7) or strychnine (glycine receptor antagonist, 10 μM, n=7); iii) the respiratory pattern of SH rats in situ (n=7) and in vivo (n=12); iv) effects on the respiratory motor activity of control (n=7) and SH rats (n=7) after microinjections of L-glutamate in BötC (10 mM); v) changes in respiratory pattern of SH rats (n=8) promoted by the pharmacological disinhibition of the BötC with strychnine (10 μM). In control rats, post-I and aug-E neurons were recorded under hypercapnia (8% CO2). Hypercapnia evoked late-E activity in the abdominal nerve (AbN), in association with a decreased post-I activity and augmented aug-E activity. Regarding to the bilateral microinjections of gabazine in the BötC of control rats, we observed a decrease in baseline phrenic nerve (PN) bursts frequency and increases in the expiratory time and in the AbN activity, with the emergence of late-E bursts. On the other hand, bilateral microinjections of strychnine in the BötC of control rats diminished the PN, vagus (cVN) and AbN nerve amplitudes, but did not modify the 3-phase respiratory pattern; and attenuated the emergence of the active expiratory pattern under hypercapnia conditions. Concerning the basal ventilatory pattern of unanesthetized SH rats, we observed an increase in minute ventilation, associated with a higher respiratory frequency and tidal volume. These findings obtained in in vivo parallel with our data from in situ preparations, showing that SH evoked active expiratory pattern at baseline conditions. BötC stimulation of SH rats with L-glutamate was able to briefly abolish AbN late-E activity. In addition, BötC disinhibition of SH animals with strychnine eliminated the late-E AbN firing and restored the respiratory motor pattern, similarly to control animals. Taken together, our results indicate that BötC perform a relevant inhibitory role on the mechanisms of active expiratory pattern generation. In addition, short-term SH seems to change the activity of BötC neurons, reducing this inhibitory drive and contributing to the emergence late-E AbN activity at resting conditions in these animals.Neurônios expiratórios tardios (late-E), localizados no grupamento respiratório parafacial (pFRG), região crítica para o padrão expiratório ativo, são condicionais, permanecendo silentes em condições basais, mas em situações de desafios metabólicos, tornam-se ativos e contribuem para o aumento da atividade motora abdominal durante a fase final da expiração (expiração ativa). Foi verificado que a inibição dos neurônios late-E, em condições basais, é mantida por um tônus inibitório. Interessante, a exposição à hipóxia sustentada (SH) parece reduzir esse drive inibitório, promovendo o surgimento da expiração ativa. No presente estudo, exploramos a possibilidade de que tal mecanismo inibitório do BötC esteja reduzido após a SH, e que a ativação desse mecanismo seria capaz de normalizar o padrão expiratório dos ratos SH. O objetivo do presente trabalho foi verificar a contribuição dos neurônios do BötC na geração do padrão de expiração ativa em ratos controle e SH (10% O2, 24 h). Para tanto, foram realizados registros da ventilação pulmonar (in vivo) e registros da atividade motora respiratória em preparações in situ de ratos jovens (60-80 g) para avaliar, em normocapnia e hipercapnia (8-10% CO2): i) o padrão de atividade dos neurônios post-I (n=5) e aug-E (n=9) do BötC de ratos controle; ii) as alterações no padrão respiratório após a desinibição farmacológica do BötC de ratos controle com gabazina (n=7) ou estriquinina (n=7); iii) o padrão respiratório de animais SH in situ (n=7) e in vivo (n=12); iv) os efeitos sobre a atividade motora respiratória de ratos controle (n=7) e SH (n=7) após microinjeções de L-glutamato no BötC; v) as alterações no padrão respiratório de ratos SH (n=8) promovidos pela desinibição farmacológica do BötC com estriquinina. Em hipercapnia, que evoca a atividade late-E no nervo abdominal (AbN), foi verificada redução no tempo de atividade dos neurônios post-I, enquanto que os neurônios aug-E apresentaram aumento no tempo em sua atividade. Em relação às microinjeções de gabazina no BötC de ratos controle foi verificada, em condições basais, redução na frequência dos bursts do nervo frênico (PN), e aumentos do tempo expiratório e da atividade AbN, com a presença de bursts late-E. Por outro lado, microinjeções de estriquinina no BötC de ratos controle promoveu redução modesta na amplitude dos nervos PN, vago (cVN) e AbN, sem modificar o padrão respiratório, e atenuou o surgimento do padrão de expiração ativa em hipercapnia. Em relação ao padrão ventilatório basal de ratos SH não anestesiados, verificamos um aumento da ventilação minuto, associado a maior frequência respiratória e volume corrente. A estimulação do BötC de animais SH foi capaz de abolir, momentaneamente, a atividade late-E AbN. Além disso, a desinibição do BötC de animais SH com estriquinina eliminou os disparos late-E AbN e restaurou o padrão motor respiratório. Em conjunto, nossos resultados indicam que o BötC exerce um papel inibitório relevante sobre os mecanismos de geração do padrão expiratório ativo. Além disso, a SH de curta duração parece modificar a atividade dos neurônios BötC, reduzindo esse drive inibitório e contribuindo para o surgimento da atividade late-E AbN, em condições basais nesses animaiConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP 2013/17.251-6FAPESP 2015/23.568-8CNPq 302892/2014-1porUniversidade Federal de São CarlosCâmpus São CarlosPrograma Interinstitucional de Pós-Graduação em Ciências Fisiológicas - PIPGCFUFSCarExpiração ativaHipóxia sustentadaBötzingerActive expirationSustained hypoxiaCIENCIAS BIOLOGICAS::FISIOLOGIAControle inibitório do padrão de expiração ativa em ratosInhibitory control of the active expiratory pattern in ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisOnline6d9b23ff-f0ff-4d58-aca1-8c3a886cda54info:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFSCARinstname:Universidade Federal de São Carlos (UFSCAR)instacron:UFSCARORIGINALDISSERTAÇÃO FINAL + ARTIGO - KARINE FLOR_DZ_FINAL (2).pdfDISSERTAÇÃO FINAL + ARTIGO - KARINE FLOR_DZ_FINAL (2).pdfDissertação de Mestrado - Karine Florapplication/pdf5973613https://repositorio.ufscar.br/bitstream/ufscar/9951/1/DISSERTAC%cc%a7A%cc%83O%20FINAL%20%2b%20ARTIGO%20-%20KARINE%20FLOR_DZ_FINAL%20%282%29.pdfd31191f20a7b5639152ecd77f0a995baMD51Carta comprovante - DANIEL ZOCCAL - KARINE FLOR.pdfCarta comprovante - DANIEL ZOCCAL - KARINE FLOR.pdfCarta comprovanteapplication/pdf182790https://repositorio.ufscar.br/bitstream/ufscar/9951/3/Carta%20comprovante%20-%20DANIEL%20ZOCCAL%20-%20KARINE%20FLOR.pdf62769cd2afe91182447dbf7cb2244edaMD53LICENSElicense.txtlicense.txttext/plain; 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dc.title.por.fl_str_mv Controle inibitório do padrão de expiração ativa em ratos
dc.title.alternative.eng.fl_str_mv Inhibitory control of the active expiratory pattern in rats
title Controle inibitório do padrão de expiração ativa em ratos
spellingShingle Controle inibitório do padrão de expiração ativa em ratos
Flor, Karine Correa
Expiração ativa
Hipóxia sustentada
Bötzinger
Active expiration
Sustained hypoxia
CIENCIAS BIOLOGICAS::FISIOLOGIA
title_short Controle inibitório do padrão de expiração ativa em ratos
title_full Controle inibitório do padrão de expiração ativa em ratos
title_fullStr Controle inibitório do padrão de expiração ativa em ratos
title_full_unstemmed Controle inibitório do padrão de expiração ativa em ratos
title_sort Controle inibitório do padrão de expiração ativa em ratos
author Flor, Karine Correa
author_facet Flor, Karine Correa
author_role author
dc.contributor.authorlattes.por.fl_str_mv http://lattes.cnpq.br/2988063599123256
dc.contributor.author.fl_str_mv Flor, Karine Correa
dc.contributor.advisor1.fl_str_mv Zoccal, Daniel Breseghello
dc.contributor.advisor1Lattes.fl_str_mv http://lattes.cnpq.br/1958567557189244
dc.contributor.authorID.fl_str_mv 4fde01e8-ca53-423c-910d-79a5c46a301c
contributor_str_mv Zoccal, Daniel Breseghello
dc.subject.por.fl_str_mv Expiração ativa
Hipóxia sustentada
Bötzinger
topic Expiração ativa
Hipóxia sustentada
Bötzinger
Active expiration
Sustained hypoxia
CIENCIAS BIOLOGICAS::FISIOLOGIA
dc.subject.eng.fl_str_mv Active expiration
Sustained hypoxia
dc.subject.cnpq.fl_str_mv CIENCIAS BIOLOGICAS::FISIOLOGIA
description Late-expiratory neurons (late-E) located in the parafacial respiratory group (pFRG), a critical region for the emergence of active expiratory pattern, are conditional and remain silent at baseline conditions. In situations of metabolic challenges, these neurons become active and contribute to increase the abdominal motor activity during the late expiratory phase. It was found that late-E neurons are silent at rest due to inhibitory inputs. Interestingly, in conditions of sustained hypoxia (SH), commonly observed in people moving to high altitudes, this inhibitory drive is reduced and generates the active expiratory pattern. In the present study we hypothesized that the Bötzinger complex (BötC), located in the ventral respiratory column, plays an important inhibitory role on the emergence of active expiration. We also explored the possibility that BötC inhibitory mechanism is reduced after SH and the activation of this mechanism is able to normalize the expiratory pattern of SH rats. The aim of the present study was to explore the contribution of the BötC neurons in the generation of the active expiratory pattern in control and SH (10% O2, 24 h) rats. To reach this goal, we recorded the pulmonary ventilation (in vivo) and respiratory motor activity in in situ preparations of juvenile rats (60-80 g) to evaluate, under normocapnic and hypercapnic (8-10% CO2) conditions: i) activity patterns of BötC post-I (n=5) and aug-E (n=9) neurons of control rats; ii) changes in the respiratory pattern after BötC pharmacological disinhibition of control rats with gabazine (GABAA receptor antagonist, 250 μM, n=7) or strychnine (glycine receptor antagonist, 10 μM, n=7); iii) the respiratory pattern of SH rats in situ (n=7) and in vivo (n=12); iv) effects on the respiratory motor activity of control (n=7) and SH rats (n=7) after microinjections of L-glutamate in BötC (10 mM); v) changes in respiratory pattern of SH rats (n=8) promoted by the pharmacological disinhibition of the BötC with strychnine (10 μM). In control rats, post-I and aug-E neurons were recorded under hypercapnia (8% CO2). Hypercapnia evoked late-E activity in the abdominal nerve (AbN), in association with a decreased post-I activity and augmented aug-E activity. Regarding to the bilateral microinjections of gabazine in the BötC of control rats, we observed a decrease in baseline phrenic nerve (PN) bursts frequency and increases in the expiratory time and in the AbN activity, with the emergence of late-E bursts. On the other hand, bilateral microinjections of strychnine in the BötC of control rats diminished the PN, vagus (cVN) and AbN nerve amplitudes, but did not modify the 3-phase respiratory pattern; and attenuated the emergence of the active expiratory pattern under hypercapnia conditions. Concerning the basal ventilatory pattern of unanesthetized SH rats, we observed an increase in minute ventilation, associated with a higher respiratory frequency and tidal volume. These findings obtained in in vivo parallel with our data from in situ preparations, showing that SH evoked active expiratory pattern at baseline conditions. BötC stimulation of SH rats with L-glutamate was able to briefly abolish AbN late-E activity. In addition, BötC disinhibition of SH animals with strychnine eliminated the late-E AbN firing and restored the respiratory motor pattern, similarly to control animals. Taken together, our results indicate that BötC perform a relevant inhibitory role on the mechanisms of active expiratory pattern generation. In addition, short-term SH seems to change the activity of BötC neurons, reducing this inhibitory drive and contributing to the emergence late-E AbN activity at resting conditions in these animals.
publishDate 2018
dc.date.accessioned.fl_str_mv 2018-05-10T14:20:39Z
dc.date.available.fl_str_mv 2018-05-10T14:20:39Z
dc.date.issued.fl_str_mv 2018-02-22
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/masterThesis
format masterThesis
status_str publishedVersion
dc.identifier.citation.fl_str_mv FLOR, Karine Correa. Controle inibitório do padrão de expiração ativa em ratos. 2018. Dissertação (Mestrado em Ciências Fisiológicas) – Universidade Federal de São Carlos, São Carlos, 2018. Disponível em: https://repositorio.ufscar.br/handle/ufscar/9951.
dc.identifier.uri.fl_str_mv https://repositorio.ufscar.br/handle/ufscar/9951
identifier_str_mv FLOR, Karine Correa. Controle inibitório do padrão de expiração ativa em ratos. 2018. Dissertação (Mestrado em Ciências Fisiológicas) – Universidade Federal de São Carlos, São Carlos, 2018. Disponível em: https://repositorio.ufscar.br/handle/ufscar/9951.
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