rdf:type |
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lifeskim:mentions |
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pubmed:issue |
Pt 3
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pubmed:dateCreated |
2005-8-3
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pubmed:abstractText |
Brainstem 5-hydroxytryptamine (5-HT, serotonin)-containing neurones modulate cardiovascular reflex responses but the differing roles of the many 5-HT receptors have not been thoroughly investigated. The present experiments on anaesthetized rats investigated the role of 5-HT3 receptors in modulating vagal afferent evoked activity of nucleus tractus solitarius (NTS) neurones. Recordings were made from 301 NTS neurones receiving an input at long (> 20 ms) minimum onset latency from stimulation of the vagus nerve. These included 140 neurones excited by activating non-myelinated cardiopulmonary afferents by right atrial injection of phenylbiguanide (PBG). Ionophoretic application of PBG, a highly selective 5-HT3 receptor agonist, significantly increased activity (from 2.4 +/- 0.4 to 5.5 +/- 0.8 spikes s(-1)) in 96 of 106 neurones tested and in all 17 neurones tested the increase in activity (3.4 +/- 1.1 to 7.0 +/- 1.9 spikes s(-1)) was significantly attenuated (3.0 +/- 0.9 to 3.8 +/- 1.1 spikes s(-1)) by the selective 5-HT3 receptor antagonist granisetron. Ionophoretic application of PBG potentiated responses to vagus nerve and cardiopulmonary afferent stimulation, and granisetron significantly attenuated this cardiopulmonary input (20.2 +/- 5.7 to 10.6 +/- 4.1 spikes burst(-1)) in 9 of 10 neurones tested. Ionophoretic application of AMPA and NMDA also excited NTS neurones and these excitations could be selectively antagonized by the non-NMDA and NMDA receptor antagonists DNQX and AP-5, respectively. At these selective currents, DNQX and AP-5 also attenuated PBG- and cardiopulmonary input-evoked increases in NTS activity. These data are consistent with the hypothesis that vagal inputs, including non-myelinated cardiopulmonary inputs to the NTS, utilize a 5-HT-containing pathway which activates 5-HT3 receptors. This excitatory response to 5-HT3 receptor activation may be partly a direct postsynaptic action but part may also be due to facilitation of the release of glutamate which in turn acts on either non-NMDA or NMDA receptors to evoke excitation.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/15905216-10390519,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15905216-10837806,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15905216-11226709,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/15905216-1585260,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/15905216-3823479,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/15905216-9542727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15905216-9593908,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/15905216-9666094,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15905216-9853906
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
566
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
939-53
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:15905216-Action Potentials,
pubmed-meshheading:15905216-Anesthesia,
pubmed-meshheading:15905216-Animals,
pubmed-meshheading:15905216-Feedback,
pubmed-meshheading:15905216-Male,
pubmed-meshheading:15905216-Neurons,
pubmed-meshheading:15905216-Rats,
pubmed-meshheading:15905216-Rats, Sprague-Dawley,
pubmed-meshheading:15905216-Receptors, Serotonin, 5-HT3,
pubmed-meshheading:15905216-Reflex,
pubmed-meshheading:15905216-Solitary Nucleus,
pubmed-meshheading:15905216-Vagus Nerve
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pubmed:year |
2005
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pubmed:articleTitle |
The role of central 5-HT3 receptors in vagal reflex inputs to neurones in the nucleus tractus solitarius of anaesthetized rats.
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pubmed:affiliation |
Department of Physiology, Royal Free and University College Medical School, Royal Free Campus, Rowland Hill St, London NW3 2PF, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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