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Plasticity in Preganglionic and Postganglionic Neurons of the Sympathetic Nervous System during Embryonic Development

Sympathetic preganglionic neurons (SPNs) are the final output neurons from the central arm of the autonomic nervous system. Therefore, SPNs represent a crucial component of the sympathetic nervous system for integrating several inputs before driving the postganglionic neurons (PGNs) in the periphery...

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Autores principales: Ratliff, April, Pekala, Dobromila, Wenner, Peter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Society for Neuroscience 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10630925/
https://www.ncbi.nlm.nih.gov/pubmed/37833062
http://dx.doi.org/10.1523/ENEURO.0297-23.2023
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author Ratliff, April
Pekala, Dobromila
Wenner, Peter
author_facet Ratliff, April
Pekala, Dobromila
Wenner, Peter
author_sort Ratliff, April
collection PubMed
description Sympathetic preganglionic neurons (SPNs) are the final output neurons from the central arm of the autonomic nervous system. Therefore, SPNs represent a crucial component of the sympathetic nervous system for integrating several inputs before driving the postganglionic neurons (PGNs) in the periphery to control end organ function. The mechanisms which establish and regulate baseline sympathetic tone and overall excitability of SPNs and PGNs are poorly understood. The SPNs are also known as the autonomic motoneurons (MNs) as they arise from the same progenitor line as somatic MNs that innervate skeletal muscles. Previously our group has identified a rich repertoire of homeostatic plasticity (HP) mechanisms in somatic MNs of the embryonic chick following in vivo synaptic blockade. Here, using the same model system, we examined whether SPNs exhibit similar homeostatic capabilities to that of somatic MNs. Indeed, we found that after 2-d reduction of excitatory synaptic input, SPNs showed a significant increase in intracellular chloride levels, the mechanism underlying GABAergic synaptic scaling in this system. This form of HP could therefore play a role in the early establishment of a setpoint of excitability in this part of the sympathetic nervous system. Next, we asked whether homeostatic mechanisms are expressed in the synaptic targets of SPNs, the PGNs. In this case we blocked synaptic input to PGNs in vivo (48-h treatment), or acutely ex vivo, however neither treatment induced homeostatic adjustments in PGN excitability. We discuss differences in the homeostatic capacity between the central and peripheral component of the sympathetic nervous system.
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spelling pubmed-106309252023-11-03 Plasticity in Preganglionic and Postganglionic Neurons of the Sympathetic Nervous System during Embryonic Development Ratliff, April Pekala, Dobromila Wenner, Peter eNeuro Research Article: New Research Sympathetic preganglionic neurons (SPNs) are the final output neurons from the central arm of the autonomic nervous system. Therefore, SPNs represent a crucial component of the sympathetic nervous system for integrating several inputs before driving the postganglionic neurons (PGNs) in the periphery to control end organ function. The mechanisms which establish and regulate baseline sympathetic tone and overall excitability of SPNs and PGNs are poorly understood. The SPNs are also known as the autonomic motoneurons (MNs) as they arise from the same progenitor line as somatic MNs that innervate skeletal muscles. Previously our group has identified a rich repertoire of homeostatic plasticity (HP) mechanisms in somatic MNs of the embryonic chick following in vivo synaptic blockade. Here, using the same model system, we examined whether SPNs exhibit similar homeostatic capabilities to that of somatic MNs. Indeed, we found that after 2-d reduction of excitatory synaptic input, SPNs showed a significant increase in intracellular chloride levels, the mechanism underlying GABAergic synaptic scaling in this system. This form of HP could therefore play a role in the early establishment of a setpoint of excitability in this part of the sympathetic nervous system. Next, we asked whether homeostatic mechanisms are expressed in the synaptic targets of SPNs, the PGNs. In this case we blocked synaptic input to PGNs in vivo (48-h treatment), or acutely ex vivo, however neither treatment induced homeostatic adjustments in PGN excitability. We discuss differences in the homeostatic capacity between the central and peripheral component of the sympathetic nervous system. Society for Neuroscience 2023-11-03 /pmc/articles/PMC10630925/ /pubmed/37833062 http://dx.doi.org/10.1523/ENEURO.0297-23.2023 Text en Copyright © 2023 Ratliff et al. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
spellingShingle Research Article: New Research
Ratliff, April
Pekala, Dobromila
Wenner, Peter
Plasticity in Preganglionic and Postganglionic Neurons of the Sympathetic Nervous System during Embryonic Development
title Plasticity in Preganglionic and Postganglionic Neurons of the Sympathetic Nervous System during Embryonic Development
title_full Plasticity in Preganglionic and Postganglionic Neurons of the Sympathetic Nervous System during Embryonic Development
title_fullStr Plasticity in Preganglionic and Postganglionic Neurons of the Sympathetic Nervous System during Embryonic Development
title_full_unstemmed Plasticity in Preganglionic and Postganglionic Neurons of the Sympathetic Nervous System during Embryonic Development
title_short Plasticity in Preganglionic and Postganglionic Neurons of the Sympathetic Nervous System during Embryonic Development
title_sort plasticity in preganglionic and postganglionic neurons of the sympathetic nervous system during embryonic development
topic Research Article: New Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10630925/
https://www.ncbi.nlm.nih.gov/pubmed/37833062
http://dx.doi.org/10.1523/ENEURO.0297-23.2023
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