Sensory neurons display cell-type-specific vulnerability to loss of neuron-glia interactions

Benayahu Elbaz; Lite Yang; Maia Vardy; Sara Isaac; Braesen L Rader; Riki Kawaguchi; Maria Traka; Clifford J Woolf; William Renthal; Brian Popko

doi:10.1016/j.celrep.2022.111130

Sensory neurons display cell-type-specific vulnerability to loss of neuron-glia interactions

Cell Rep. 2022 Jul 19;40(3):111130. doi: 10.1016/j.celrep.2022.111130.

Authors

Affiliations

¹ Department of Neurology, Northwestern Feinberg School of Medicine, Chicago, IL, USA. Electronic address: benayahu.elbaz-eilon@northwestern.edu.
² Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Road, Boston, MA 02115, USA.
³ Department of Neurology, Northwestern Feinberg School of Medicine, Chicago, IL, USA.
⁴ Department of Cell and Developmental Biology, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
⁵ Program in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
⁶ Department of Anatomy, College of Graduate Studies, Midwestern University, Downers Grove, IL, USA.
⁷ Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; F.M. Kirby Neurobiology Center, Boston Children's Hospital, 3 Blackfan Circle, Boston, MA 02115, USA.
⁸ Department of Neurology, Northwestern Feinberg School of Medicine, Chicago, IL, USA. Electronic address: brian.popko@northwestern.edu.

Abstract

Peripheral nervous system (PNS) injuries initiate transcriptional changes in glial cells and sensory neurons that promote axonal regeneration. While the factors that initiate the transcriptional changes in glial cells are well characterized, the full range of stimuli that initiate the response of sensory neurons remain elusive. Here, using a genetic model of glial cell ablation, we find that glial cell loss results in transient PNS demyelination without overt axonal loss. By profiling sensory ganglia at single-cell resolution, we show that glial cell loss induces a transcriptional injury response preferentially in proprioceptive and Aβ RA-LTMR neurons. The transcriptional response of sensory neurons to mechanical injury has been assumed to be a cell-autonomous response. By identifying a similar response in non-injured, demyelinated neurons, our study suggests that this represents a non-cell-autonomous transcriptional response of sensory neurons to glial cell loss and demyelination.

Keywords: CP: Neuroscience.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

Demyelinating Diseases*
Humans
Neuroglia* / physiology
Peripheral Nervous System
Sensory Receptor Cells

Abstract

Publication types

MeSH terms

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