Modulation of hypercapnic respiratory response by cholinergic transmission in the commissural nucleus of the solitary tract
The nucleus of the solitary tract (NTS) is an important area of the brainstem that receives and integrates afferent cardiorespiratory sensorial information, including those from arterial chemoreceptors and baroreceptors. It was described that acetylcholine (ACh) in the commissural subnucleus of the...
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| Veröffentlicht in: | Pflügers Archiv 2020, Vol.472 (1), p.49-60 |
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| description | The nucleus of the solitary tract (NTS) is an important area of the brainstem that receives and integrates afferent cardiorespiratory sensorial information, including those from arterial chemoreceptors and baroreceptors. It was described that acetylcholine (ACh) in the commissural subnucleus of the NTS (cNTS) promotes an increase in the phrenic nerve activity (PNA) and antagonism of nicotinic receptors in the same region reduces the magnitude of tachypneic response to peripheral chemoreceptor stimulation, suggesting a functional role of cholinergic transmission within the cNTS in the chemosensory control of respiratory activity. In the present study, we investigated whether cholinergic receptor antagonism in the cNTS modifies the sympathetic and respiratory reflex responses to hypercapnia. Using an arterially perfused in situ preparation of juvenile male Holtzman rats, we found that the nicotinic antagonist (mecamylamine, 5 mM), but not the muscarinic antagonist (atropine, 5 mM), into the cNTS attenuated the hypercapnia-induced increase of hypoglossal activity. Furthermore, mecamylamine in the cNTS potentiated the generation of late-expiratory (late-E) activity in abdominal nerve induced by hypercapnia. None of the cholinergic antagonists microinjected in the cNTS changed either the sympathetic or the phrenic nerve responses to hypercapnia. Our data provide evidence for the role of cholinergic transmission in the cNTS, acting on nicotinic receptors, modulating the hypoglossal and abdominal responses to hypercapnia. |
| doi_str_mv | 10.1007/s00424-019-02341-9 |
| format | Article |
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A.</creator><creatorcontrib>Furuya, Werner I. ; Bassi, Mirian ; Menani, José V. ; Colombari, Eduardo ; Zoccal, Daniel B. ; Colombari, Débora S. A.</creatorcontrib><description>The nucleus of the solitary tract (NTS) is an important area of the brainstem that receives and integrates afferent cardiorespiratory sensorial information, including those from arterial chemoreceptors and baroreceptors. It was described that acetylcholine (ACh) in the commissural subnucleus of the NTS (cNTS) promotes an increase in the phrenic nerve activity (PNA) and antagonism of nicotinic receptors in the same region reduces the magnitude of tachypneic response to peripheral chemoreceptor stimulation, suggesting a functional role of cholinergic transmission within the cNTS in the chemosensory control of respiratory activity. In the present study, we investigated whether cholinergic receptor antagonism in the cNTS modifies the sympathetic and respiratory reflex responses to hypercapnia. Using an arterially perfused in situ preparation of juvenile male Holtzman rats, we found that the nicotinic antagonist (mecamylamine, 5 mM), but not the muscarinic antagonist (atropine, 5 mM), into the cNTS attenuated the hypercapnia-induced increase of hypoglossal activity. Furthermore, mecamylamine in the cNTS potentiated the generation of late-expiratory (late-E) activity in abdominal nerve induced by hypercapnia. None of the cholinergic antagonists microinjected in the cNTS changed either the sympathetic or the phrenic nerve responses to hypercapnia. Our data provide evidence for the role of cholinergic transmission in the cNTS, acting on nicotinic receptors, modulating the hypoglossal and abdominal responses to hypercapnia.</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s00424-019-02341-9</identifier><identifier>PMID: 31884528</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Acetylcholine ; Acetylcholine receptors ; Acetylcholine receptors (muscarinic) ; Acetylcholine receptors (nicotinic) ; Animals ; Atropine ; Atropine - pharmacology ; Baroreceptors ; Biomedical and Life Sciences ; Biomedicine ; Brain stem ; Cell Biology ; Chemoreception ; Chemoreceptors (internal) ; Cholinergic Neurons - drug effects ; Cholinergic Neurons - physiology ; Cholinergic transmission ; Human Physiology ; Hypercapnia ; Hypercapnia - metabolism ; Hypercapnia - physiopathology ; Hypoglossal Nerve - physiology ; Integrative Physiology ; Male ; Mecamylamine ; Mecamylamine - pharmacology ; Molecular Medicine ; Muscarinic Agonists - pharmacology ; Neurosciences ; Nicotinic Antagonists - pharmacology ; Phrenic nerve ; Phrenic Nerve - physiology ; Rats ; Receptors ; Receptors, Cholinergic - metabolism ; Reflex ; Respiration ; Sensory neurons ; Solitary Nucleus - physiology ; Solitary Nucleus - physiopathology ; Solitary tract nucleus ; Synaptic Transmission ; Telencephalic Commissures - physiology ; Telencephalic Commissures - physiopathology</subject><ispartof>Pflügers Archiv, 2020, Vol.472 (1), p.49-60</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2019</rights><rights>Pflügers Archiv - European Journal of Physiology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-1257c06cb178c736530bcdfc9f776570a4b4f18290d0149faeb22ca347c0c5e13</citedby><cites>FETCH-LOGICAL-c375t-1257c06cb178c736530bcdfc9f776570a4b4f18290d0149faeb22ca347c0c5e13</cites><orcidid>0000-0002-0369-5907 ; 0000-0003-1167-4441 ; 0000-0002-1395-4036 ; 0000-0003-4331-0271</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00424-019-02341-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00424-019-02341-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31884528$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Furuya, Werner I.</creatorcontrib><creatorcontrib>Bassi, Mirian</creatorcontrib><creatorcontrib>Menani, José V.</creatorcontrib><creatorcontrib>Colombari, Eduardo</creatorcontrib><creatorcontrib>Zoccal, Daniel B.</creatorcontrib><creatorcontrib>Colombari, Débora S. A.</creatorcontrib><title>Modulation of hypercapnic respiratory response by cholinergic transmission in the commissural nucleus of the solitary tract</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch - Eur J Physiol</addtitle><addtitle>Pflugers Arch</addtitle><description>The nucleus of the solitary tract (NTS) is an important area of the brainstem that receives and integrates afferent cardiorespiratory sensorial information, including those from arterial chemoreceptors and baroreceptors. It was described that acetylcholine (ACh) in the commissural subnucleus of the NTS (cNTS) promotes an increase in the phrenic nerve activity (PNA) and antagonism of nicotinic receptors in the same region reduces the magnitude of tachypneic response to peripheral chemoreceptor stimulation, suggesting a functional role of cholinergic transmission within the cNTS in the chemosensory control of respiratory activity. In the present study, we investigated whether cholinergic receptor antagonism in the cNTS modifies the sympathetic and respiratory reflex responses to hypercapnia. Using an arterially perfused in situ preparation of juvenile male Holtzman rats, we found that the nicotinic antagonist (mecamylamine, 5 mM), but not the muscarinic antagonist (atropine, 5 mM), into the cNTS attenuated the hypercapnia-induced increase of hypoglossal activity. Furthermore, mecamylamine in the cNTS potentiated the generation of late-expiratory (late-E) activity in abdominal nerve induced by hypercapnia. None of the cholinergic antagonists microinjected in the cNTS changed either the sympathetic or the phrenic nerve responses to hypercapnia. Our data provide evidence for the role of cholinergic transmission in the cNTS, acting on nicotinic receptors, modulating the hypoglossal and abdominal responses to hypercapnia.</description><subject>Acetylcholine</subject><subject>Acetylcholine receptors</subject><subject>Acetylcholine receptors (muscarinic)</subject><subject>Acetylcholine receptors (nicotinic)</subject><subject>Animals</subject><subject>Atropine</subject><subject>Atropine - pharmacology</subject><subject>Baroreceptors</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain stem</subject><subject>Cell Biology</subject><subject>Chemoreception</subject><subject>Chemoreceptors (internal)</subject><subject>Cholinergic Neurons - drug effects</subject><subject>Cholinergic Neurons - physiology</subject><subject>Cholinergic transmission</subject><subject>Human Physiology</subject><subject>Hypercapnia</subject><subject>Hypercapnia - metabolism</subject><subject>Hypercapnia - physiopathology</subject><subject>Hypoglossal Nerve - physiology</subject><subject>Integrative Physiology</subject><subject>Male</subject><subject>Mecamylamine</subject><subject>Mecamylamine - pharmacology</subject><subject>Molecular Medicine</subject><subject>Muscarinic Agonists - pharmacology</subject><subject>Neurosciences</subject><subject>Nicotinic Antagonists - pharmacology</subject><subject>Phrenic nerve</subject><subject>Phrenic Nerve - physiology</subject><subject>Rats</subject><subject>Receptors</subject><subject>Receptors, Cholinergic - metabolism</subject><subject>Reflex</subject><subject>Respiration</subject><subject>Sensory neurons</subject><subject>Solitary Nucleus - physiology</subject><subject>Solitary Nucleus - physiopathology</subject><subject>Solitary tract nucleus</subject><subject>Synaptic Transmission</subject><subject>Telencephalic Commissures - physiology</subject><subject>Telencephalic Commissures - physiopathology</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kTtPwzAYRS0EoqXwBxhQJBaWwOdHYmdEiJdUxAKz5bhOmyq1g50MFX8epykgMTDZ8nfOta2L0DmGawzAbwIAIywFXKRAKMNpcYCmmFGSEsD0EE0BKE5znosJOglhDQCECXKMJhQLwTIipujzxS36RnW1s4mrktW2NV6r1tY68Sa0tVed89vd3tlgknKb6JVramv8MjKdVzZs6hAGv7ZJtzKJdpvhpPeqSWyvG9OHIXoYhWh2KuZFT3en6KhSTTBn-3WG3h_u3-6e0vnr4_Pd7TzVlGddiknGNeS6xFxoTvOMQqkXlS4qzvOMg2Ilq7AgBSwAs6JSpiREK8qipTOD6Qxdjbmtdx-9CZ2M79OmaZQ1rg-SUIoZKVjGInr5B1273tv4ukgxKoggQCNFRkp7F4I3lWx9vYn_khjkUI0cq5GxGrmrRhZRuthH9-XGLH6U7y4iQEcgxJFdGv979z-xX11rm40</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Furuya, Werner I.</creator><creator>Bassi, Mirian</creator><creator>Menani, José V.</creator><creator>Colombari, Eduardo</creator><creator>Zoccal, Daniel B.</creator><creator>Colombari, Débora S. 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A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-1257c06cb178c736530bcdfc9f776570a4b4f18290d0149faeb22ca347c0c5e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acetylcholine</topic><topic>Acetylcholine receptors</topic><topic>Acetylcholine receptors (muscarinic)</topic><topic>Acetylcholine receptors (nicotinic)</topic><topic>Animals</topic><topic>Atropine</topic><topic>Atropine - pharmacology</topic><topic>Baroreceptors</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain stem</topic><topic>Cell Biology</topic><topic>Chemoreception</topic><topic>Chemoreceptors (internal)</topic><topic>Cholinergic Neurons - drug effects</topic><topic>Cholinergic Neurons - physiology</topic><topic>Cholinergic transmission</topic><topic>Human Physiology</topic><topic>Hypercapnia</topic><topic>Hypercapnia - metabolism</topic><topic>Hypercapnia - physiopathology</topic><topic>Hypoglossal Nerve - physiology</topic><topic>Integrative Physiology</topic><topic>Male</topic><topic>Mecamylamine</topic><topic>Mecamylamine - pharmacology</topic><topic>Molecular Medicine</topic><topic>Muscarinic Agonists - pharmacology</topic><topic>Neurosciences</topic><topic>Nicotinic Antagonists - pharmacology</topic><topic>Phrenic nerve</topic><topic>Phrenic Nerve - physiology</topic><topic>Rats</topic><topic>Receptors</topic><topic>Receptors, Cholinergic - metabolism</topic><topic>Reflex</topic><topic>Respiration</topic><topic>Sensory neurons</topic><topic>Solitary Nucleus - physiology</topic><topic>Solitary Nucleus - physiopathology</topic><topic>Solitary tract nucleus</topic><topic>Synaptic Transmission</topic><topic>Telencephalic Commissures - physiology</topic><topic>Telencephalic Commissures - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Furuya, Werner I.</creatorcontrib><creatorcontrib>Bassi, Mirian</creatorcontrib><creatorcontrib>Menani, José V.</creatorcontrib><creatorcontrib>Colombari, Eduardo</creatorcontrib><creatorcontrib>Zoccal, Daniel B.</creatorcontrib><creatorcontrib>Colombari, Débora S. 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A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of hypercapnic respiratory response by cholinergic transmission in the commissural nucleus of the solitary tract</atitle><jtitle>Pflügers Archiv</jtitle><stitle>Pflugers Arch - Eur J Physiol</stitle><addtitle>Pflugers Arch</addtitle><date>2020</date><risdate>2020</risdate><volume>472</volume><issue>1</issue><spage>49</spage><epage>60</epage><pages>49-60</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>The nucleus of the solitary tract (NTS) is an important area of the brainstem that receives and integrates afferent cardiorespiratory sensorial information, including those from arterial chemoreceptors and baroreceptors. It was described that acetylcholine (ACh) in the commissural subnucleus of the NTS (cNTS) promotes an increase in the phrenic nerve activity (PNA) and antagonism of nicotinic receptors in the same region reduces the magnitude of tachypneic response to peripheral chemoreceptor stimulation, suggesting a functional role of cholinergic transmission within the cNTS in the chemosensory control of respiratory activity. In the present study, we investigated whether cholinergic receptor antagonism in the cNTS modifies the sympathetic and respiratory reflex responses to hypercapnia. Using an arterially perfused in situ preparation of juvenile male Holtzman rats, we found that the nicotinic antagonist (mecamylamine, 5 mM), but not the muscarinic antagonist (atropine, 5 mM), into the cNTS attenuated the hypercapnia-induced increase of hypoglossal activity. Furthermore, mecamylamine in the cNTS potentiated the generation of late-expiratory (late-E) activity in abdominal nerve induced by hypercapnia. None of the cholinergic antagonists microinjected in the cNTS changed either the sympathetic or the phrenic nerve responses to hypercapnia. Our data provide evidence for the role of cholinergic transmission in the cNTS, acting on nicotinic receptors, modulating the hypoglossal and abdominal responses to hypercapnia.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>31884528</pmid><doi>10.1007/s00424-019-02341-9</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-0369-5907</orcidid><orcidid>https://orcid.org/0000-0003-1167-4441</orcidid><orcidid>https://orcid.org/0000-0002-1395-4036</orcidid><orcidid>https://orcid.org/0000-0003-4331-0271</orcidid></addata></record> |
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| subjects | Acetylcholine Acetylcholine receptors Acetylcholine receptors (muscarinic) Acetylcholine receptors (nicotinic) Animals Atropine Atropine - pharmacology Baroreceptors Biomedical and Life Sciences Biomedicine Brain stem Cell Biology Chemoreception Chemoreceptors (internal) Cholinergic Neurons - drug effects Cholinergic Neurons - physiology Cholinergic transmission Human Physiology Hypercapnia Hypercapnia - metabolism Hypercapnia - physiopathology Hypoglossal Nerve - physiology Integrative Physiology Male Mecamylamine Mecamylamine - pharmacology Molecular Medicine Muscarinic Agonists - pharmacology Neurosciences Nicotinic Antagonists - pharmacology Phrenic nerve Phrenic Nerve - physiology Rats Receptors Receptors, Cholinergic - metabolism Reflex Respiration Sensory neurons Solitary Nucleus - physiology Solitary Nucleus - physiopathology Solitary tract nucleus Synaptic Transmission Telencephalic Commissures - physiology Telencephalic Commissures - physiopathology |
| title | Modulation of hypercapnic respiratory response by cholinergic transmission in the commissural nucleus of the solitary tract |
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