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Status: Bibliographieeintrag

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Verfasst von:Benedetti, Bruno [VerfasserIn]   i
 Bieler, Lara [VerfasserIn]   i
 Erhardt-Kreutzer, Christina [VerfasserIn]   i
 Jakubecova, Dominika [VerfasserIn]   i
 Benedetti, Ariane [VerfasserIn]   i
 Reisinger, Maximilian [VerfasserIn]   i
 Dannehl, Dominik [VerfasserIn]   i
 Thome, Christian [VerfasserIn]   i
 Engelhardt, Maren [VerfasserIn]   i
 Couillard-Despres, Sebastien [VerfasserIn]   i
Titel:Depolarization and hyperexcitability of cortical motor neurons after spinal cord injury associates with reduced HCN channel activity
Verf.angabe:Bruno Benedetti, Lara Bieler, Christina Erhardt-Kreutzer, Dominika Jakubecova, Ariane Benedetti, Maximilian Reisinger, Dominik Dannehl, Christian Thome, Maren Engelhardt and Sebastien Couillard-Despres
E-Jahr:2023
Jahr:1 March 2023
Umfang:14 S.
Fussnoten:Gesehen am 22.05.2024
Titel Quelle:Enthalten in: International journal of molecular sciences
Ort Quelle:Basel : Molecular Diversity Preservation International, 2000
Jahr Quelle:2023
Band/Heft Quelle:24(2023), 5 vom: März, Seite 1-14
ISSN Quelle:1422-0067
 1661-6596
Abstract:A spinal cord injury (SCI) damages the axonal projections of neurons residing in the neocortex. This axotomy changes cortical excitability and results in dysfunctional activity and output of infragranular cortical layers. Thus, addressing cortical pathophysiology after SCI will be instrumental in promoting recovery. However, the cellular and molecular mechanisms of cortical dysfunction after SCI are poorly resolved. In this study, we determined that the principal neurons of the primary motor cortex layer V (M1LV), those suffering from axotomy upon SCI, become hyperexcitable following injury. Therefore, we questioned the role of hyperpolarization cyclic nucleotide gated channels (HCN channels) in this context. Patch clamp experiments on axotomized M1LV neurons and acute pharmacological manipulation of HCN channels allowed us to resolve a dysfunctional mechanism controlling intrinsic neuronal excitability one week after SCI. Some axotomized M1LV neurons became excessively depolarized. In those cells, the HCN channels were less active and less relevant to control neuronal excitability because the membrane potential exceeded the window of HCN channel activation. Care should be taken when manipulating HCN channels pharmacologically after SCI. Even though the dysfunction of HCN channels partakes in the pathophysiology of axotomized M1LV neurons, their dysfunctional contribution varies remarkably between neurons and combines with other pathophysiological mechanisms.
DOI:doi:10.3390/ijms24054715
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

kostenfrei: Volltext: https://doi.org/10.3390/ijms24054715
 kostenfrei: Volltext: https://www.mdpi.com/1422-0067/24/5/4715
 DOI: https://doi.org/10.3390/ijms24054715
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:axotomy
 corticospinal tract
 HCN channels
 primary motor cortex
 spinal cord injury
K10plus-PPN:1889490970
Verknüpfungen:→ Zeitschrift

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