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Article: Activation of 5-HT7 receptors reverses NMDA receptor-dependent LTD by activating PKA at medial vestibular neurons

TitleActivation of 5-HT7 receptors reverses NMDA receptor-dependent LTD by activating PKA at medial vestibular neurons
Authors
Issue Date2017
PublisherElsevier. The Journal's web site is located at http://www.elsevier.com/locate/neuropharm
Citation
Neuropharmacology, 2017, v. 123, p. 242-248 How to Cite?
AbstractThe medial vestibular nucleus (MVN) is a major output station for neurons that project to the vestibulo-spinal pathway. MVN neurons show capacity for long-term depression (LTD) during the juvenile period. We investigated LTD of MVN neurons using whole-cell patch-clamp recordings. High frequency stimulation (HFS) robustly induced LTD in 90% of type B neurons in the MVN, while only 10% of type A neurons were responsive, indicating that type B neurons are the major contributors to LTD in the MVN. The neuromodulator serotonin (5-HT) is known to modulate LTD in neural circuits of the cerebral cortex and the hippocampus. We therefore aim to determine the action of 5-HT on the LTD of type B MVN neurons and elucidate the relevant 5-HT receptor subtypes responsible for its action. Using specific agonists and antagonists of 5-HT receptors, we found that selective activation of 5-HT7 receptor in type B neurons in the MVN of juvenile (P13-16) rats completely abolished NMDA-receptor-mediated LTD in a protein kinase A (PKA)-dependent manner. Our finding that 5-HT restricts plasticity of type B MVN neurons via 5-HT7 receptors offers a mechanism whereby vestibular tuning contributes to the maturation of the vestibulo-spinal circuit and highlights the role of 5-HT in postural control.
Persistent Identifierhttp://hdl.handle.net/10722/244667
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHan, L-
dc.contributor.authorLi, YH-
dc.contributor.authorWu, LK-
dc.contributor.authorChan, YS-
dc.date.accessioned2017-09-18T01:56:50Z-
dc.date.available2017-09-18T01:56:50Z-
dc.date.issued2017-
dc.identifier.citationNeuropharmacology, 2017, v. 123, p. 242-248-
dc.identifier.urihttp://hdl.handle.net/10722/244667-
dc.description.abstractThe medial vestibular nucleus (MVN) is a major output station for neurons that project to the vestibulo-spinal pathway. MVN neurons show capacity for long-term depression (LTD) during the juvenile period. We investigated LTD of MVN neurons using whole-cell patch-clamp recordings. High frequency stimulation (HFS) robustly induced LTD in 90% of type B neurons in the MVN, while only 10% of type A neurons were responsive, indicating that type B neurons are the major contributors to LTD in the MVN. The neuromodulator serotonin (5-HT) is known to modulate LTD in neural circuits of the cerebral cortex and the hippocampus. We therefore aim to determine the action of 5-HT on the LTD of type B MVN neurons and elucidate the relevant 5-HT receptor subtypes responsible for its action. Using specific agonists and antagonists of 5-HT receptors, we found that selective activation of 5-HT7 receptor in type B neurons in the MVN of juvenile (P13-16) rats completely abolished NMDA-receptor-mediated LTD in a protein kinase A (PKA)-dependent manner. Our finding that 5-HT restricts plasticity of type B MVN neurons via 5-HT7 receptors offers a mechanism whereby vestibular tuning contributes to the maturation of the vestibulo-spinal circuit and highlights the role of 5-HT in postural control.-
dc.languageeng-
dc.publisherElsevier. The Journal's web site is located at http://www.elsevier.com/locate/neuropharm-
dc.relation.ispartofNeuropharmacology-
dc.rightsPosting accepted manuscript (postprint): © <year>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.titleActivation of 5-HT7 receptors reverses NMDA receptor-dependent LTD by activating PKA at medial vestibular neurons-
dc.typeArticle-
dc.identifier.emailHan, L: rahanlei@hku.hk-
dc.identifier.emailWu, LK: lwu03@hku.hk-
dc.identifier.emailChan, YS: yschan@hku.hk-
dc.identifier.authorityChan, YS=rp00318-
dc.identifier.doi10.1016/j.neuropharm.2017.05.005-
dc.identifier.hkuros277822-
dc.identifier.hkuros278113-
dc.identifier.volume123-
dc.identifier.spage242-
dc.identifier.epage248-
dc.identifier.isiWOS:000406987300022-

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