Central inspiratory activity rhythmically activates synaptic currents of airway vagal preganglionic neurons in neonatal rats
Crown Copyright © 2018. Published by Elsevier B.V. All rights reserved..
The airway vagal preganglionic neurons (AVPNs) in the external formation of the nucleus ambiguus (eNA) can be separated into inspiratory-activated AVPNs (IA-AVPNs) and inspiratory-inhibited AVPNs (II-AVPNs). IA-AVPNs are activated by excitatory presynaptic inputs during inspiratory bursts, but the composition and the roles of these excitatory inputs still remain obscure. II-AVPNs are inhibited by inhibitory presynaptic inputs but whether these inhibitory inputs are regulated by excitatory inputs is also unclear. In the current study, AVPNs were retrogradely fluorescent labeled. The IA-AVPNs were discriminated from II-AVPNs by their different synaptic inputs during inspiratory bursts. The excitatory inputs to IA-AVPNs and the presynaptic regulation of II-AVPNs were examined by whole-cell patch clamping. Topical application of 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX) to the recorded IA-AVPNs almost abolished the tonic EPSCs during inspiratory intervals, inhibited the phasic excitatory currents during inspiratory bursts and attenuated the phasic inspiratory inward currents (PIICs) driven by central inspiratory activity. Blockade of α4β2 and α7 nicotinic acetylcholine receptors (nAChRs) respectively inhibited PIICs in some IA-AVPNs. Carbenoxolone, a gap junction uncoupler, partly inhibited the PIICs of IA-AVPNs. Focal application of CNQX to the II-AVPNs significantly inhibited the frequency, peak amplitude and area of the phasic inspiratory outward currents (PIOCs). These findings demonstrated that glutamatergic non-NMDA receptors played a predominant role in the excitatory drive to the IA-AVPNs, and that α4β2, α7 nAChRs and gap junctions were also rhythmically activated by central inspiratory activity. Additionally, glycinergic neurons making inhibitory inputs to the II-AVPNs were pre-synaptically facilitated by excitatory glutamatergic synaptic inputs.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2019 |
|---|---|
| Erschienen: |
2019 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:694 |
|---|---|
| Enthalten in: |
Neuroscience letters - 694(2019) vom: 16. Feb., Seite 231-237 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Hou, Lili [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 21.06.2019 Date Revised 21.06.2019 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.neulet.2018.11.024 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM290898277 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM290898277 | ||
| 003 | DE-627 | ||
| 005 | 20231225065719.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231225s2019 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.neulet.2018.11.024 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n0969.xml |
| 035 | |a (DE-627)NLM290898277 | ||
| 035 | |a (NLM)30458215 | ||
| 035 | |a (PII)S0304-3940(18)30811-5 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Hou, Lili |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Central inspiratory activity rhythmically activates synaptic currents of airway vagal preganglionic neurons in neonatal rats |
| 264 | 1 | |c 2019 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 21.06.2019 | ||
| 500 | |a Date Revised 21.06.2019 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Crown Copyright © 2018. Published by Elsevier B.V. All rights reserved. | ||
| 520 | |a The airway vagal preganglionic neurons (AVPNs) in the external formation of the nucleus ambiguus (eNA) can be separated into inspiratory-activated AVPNs (IA-AVPNs) and inspiratory-inhibited AVPNs (II-AVPNs). IA-AVPNs are activated by excitatory presynaptic inputs during inspiratory bursts, but the composition and the roles of these excitatory inputs still remain obscure. II-AVPNs are inhibited by inhibitory presynaptic inputs but whether these inhibitory inputs are regulated by excitatory inputs is also unclear. In the current study, AVPNs were retrogradely fluorescent labeled. The IA-AVPNs were discriminated from II-AVPNs by their different synaptic inputs during inspiratory bursts. The excitatory inputs to IA-AVPNs and the presynaptic regulation of II-AVPNs were examined by whole-cell patch clamping. Topical application of 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX) to the recorded IA-AVPNs almost abolished the tonic EPSCs during inspiratory intervals, inhibited the phasic excitatory currents during inspiratory bursts and attenuated the phasic inspiratory inward currents (PIICs) driven by central inspiratory activity. Blockade of α4β2 and α7 nicotinic acetylcholine receptors (nAChRs) respectively inhibited PIICs in some IA-AVPNs. Carbenoxolone, a gap junction uncoupler, partly inhibited the PIICs of IA-AVPNs. Focal application of CNQX to the II-AVPNs significantly inhibited the frequency, peak amplitude and area of the phasic inspiratory outward currents (PIOCs). These findings demonstrated that glutamatergic non-NMDA receptors played a predominant role in the excitatory drive to the IA-AVPNs, and that α4β2, α7 nAChRs and gap junctions were also rhythmically activated by central inspiratory activity. Additionally, glycinergic neurons making inhibitory inputs to the II-AVPNs were pre-synaptically facilitated by excitatory glutamatergic synaptic inputs | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Airway vagal preganglionic neurons | |
| 650 | 4 | |a Gap junctions | |
| 650 | 4 | |a N-methyl-d-aspartate | |
| 650 | 4 | |a Nicotinic acetylcholine receptor | |
| 650 | 4 | |a Non-N-methyl-d-aspartate | |
| 650 | 4 | |a Patch clamp | |
| 650 | 4 | |a Synaptic transmission | |
| 650 | 7 | |a Receptors, Nicotinic |2 NLM | |
| 650 | 7 | |a alpha7 Nicotinic Acetylcholine Receptor |2 NLM | |
| 650 | 7 | |a nicotinic receptor alpha4beta2 |2 NLM | |
| 700 | 1 | |a Bellingham, Mark C |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Yong |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Pengyu |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Xin |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Min |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Neuroscience letters |d 1975 |g 694(2019) vom: 16. Feb., Seite 231-237 |w (DE-627)NLM000386529 |x 1872-7972 |7 nnns |
| 773 | 1 | 8 | |g volume:694 |g year:2019 |g day:16 |g month:02 |g pages:231-237 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.neulet.2018.11.024 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 694 |j 2019 |b 16 |c 02 |h 231-237 | ||