Membrane lipid nanodomains modulate HCN pacemaker channels in nociceptor DRG neurons

Abstract Cell membranes consist of heterogeneous lipid nanodomains that influence key cellular processes. Using FRET-based fluorescent assays and fluorescence lifetime imaging microscopy (FLIM), we find that the dimension of cholesterol-enriched ordered membrane domains (OMD) varies considerably, de...

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Main Authors: Lucas J. Handlin, Natalie L. Macchi, Nicolas L. A. Dumaire, Lyuba Salih, Erin N. Lessie, Kyle S. McCommis, Aubin Moutal, Gucan Dai
Format: Article
Language:English
Published: Nature Portfolio 2024-11-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-024-54053-z
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author Lucas J. Handlin
Natalie L. Macchi
Nicolas L. A. Dumaire
Lyuba Salih
Erin N. Lessie
Kyle S. McCommis
Aubin Moutal
Gucan Dai
author_facet Lucas J. Handlin
Natalie L. Macchi
Nicolas L. A. Dumaire
Lyuba Salih
Erin N. Lessie
Kyle S. McCommis
Aubin Moutal
Gucan Dai
author_sort Lucas J. Handlin
collection DOAJ
description Abstract Cell membranes consist of heterogeneous lipid nanodomains that influence key cellular processes. Using FRET-based fluorescent assays and fluorescence lifetime imaging microscopy (FLIM), we find that the dimension of cholesterol-enriched ordered membrane domains (OMD) varies considerably, depending on specific cell types. Particularly, nociceptor dorsal root ganglion (DRG) neurons exhibit large OMDs. Disruption of OMDs potentiated action potential firing in nociceptor DRG neurons and facilitated the opening of native hyperpolarization-activated cyclic nucleotide-gated (HCN) pacemaker channels. This increased neuronal firing is partially due to an increased open probability and altered gating kinetics of HCN channels. The gating effect on HCN channels is likely due to a direct modulation of their voltage sensors by OMDs. In animal models of neuropathic pain, we observe reduced OMD size and a loss of HCN channel localization within OMDs. Additionally, cholesterol supplementation inhibited HCN channels and reduced neuronal hyperexcitability in pain models. These findings suggest that disturbances in lipid nanodomains play a critical role in regulating HCN channels within nociceptor DRG neurons, influencing pain modulation.
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spelling doaj-art-fad39d75223c4dd28e6df44fc3615e592024-11-17T12:36:23ZengNature PortfolioNature Communications2041-17232024-11-0115112010.1038/s41467-024-54053-zMembrane lipid nanodomains modulate HCN pacemaker channels in nociceptor DRG neuronsLucas J. Handlin0Natalie L. Macchi1Nicolas L. A. Dumaire2Lyuba Salih3Erin N. Lessie4Kyle S. McCommis5Aubin Moutal6Gucan Dai7Edward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of MedicineEdward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of MedicineDepartment of Pharmacology and Physiology, Saint Louis University School of MedicineDepartment of Pharmacology and Physiology, Saint Louis University School of MedicineEdward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of MedicineEdward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of MedicineDepartment of Pharmacology and Physiology, Saint Louis University School of MedicineEdward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of MedicineAbstract Cell membranes consist of heterogeneous lipid nanodomains that influence key cellular processes. Using FRET-based fluorescent assays and fluorescence lifetime imaging microscopy (FLIM), we find that the dimension of cholesterol-enriched ordered membrane domains (OMD) varies considerably, depending on specific cell types. Particularly, nociceptor dorsal root ganglion (DRG) neurons exhibit large OMDs. Disruption of OMDs potentiated action potential firing in nociceptor DRG neurons and facilitated the opening of native hyperpolarization-activated cyclic nucleotide-gated (HCN) pacemaker channels. This increased neuronal firing is partially due to an increased open probability and altered gating kinetics of HCN channels. The gating effect on HCN channels is likely due to a direct modulation of their voltage sensors by OMDs. In animal models of neuropathic pain, we observe reduced OMD size and a loss of HCN channel localization within OMDs. Additionally, cholesterol supplementation inhibited HCN channels and reduced neuronal hyperexcitability in pain models. These findings suggest that disturbances in lipid nanodomains play a critical role in regulating HCN channels within nociceptor DRG neurons, influencing pain modulation.https://doi.org/10.1038/s41467-024-54053-z
spellingShingle Lucas J. Handlin
Natalie L. Macchi
Nicolas L. A. Dumaire
Lyuba Salih
Erin N. Lessie
Kyle S. McCommis
Aubin Moutal
Gucan Dai
Membrane lipid nanodomains modulate HCN pacemaker channels in nociceptor DRG neurons
Nature Communications
title Membrane lipid nanodomains modulate HCN pacemaker channels in nociceptor DRG neurons
title_full Membrane lipid nanodomains modulate HCN pacemaker channels in nociceptor DRG neurons
title_fullStr Membrane lipid nanodomains modulate HCN pacemaker channels in nociceptor DRG neurons
title_full_unstemmed Membrane lipid nanodomains modulate HCN pacemaker channels in nociceptor DRG neurons
title_short Membrane lipid nanodomains modulate HCN pacemaker channels in nociceptor DRG neurons
title_sort membrane lipid nanodomains modulate hcn pacemaker channels in nociceptor drg neurons
url https://doi.org/10.1038/s41467-024-54053-z
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