Journal Article

DZNE-2020-06367

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png CNS myeloid cells critically regulate heat hyperalgesia.

Kälin, S. ; Miller, K. R. ; Kälin, R. E. ; Jendrach, M. ; Witzel, C. ; Heppner, F. L. (Last author)DZNE*

2018
ASCJ Ann Arbor, Mich.

This record in other databases:    

Please use a persistent id in citations: doi:10.1172/JCI95305

Abstract: Activation of non-neuronal microglia is thought to play a causal role in spinal processing of neuropathic pain. To specifically investigate microglia-mediated effects in a model of neuropathic pain and overcome the methodological limitations of previous approaches exploring microglia function upon nerve injury, we selectively ablated resident microglia by intracerebroventricular ganciclovir infusion into male CD11b-HSVTK-transgenic mice, which was followed by a rapid, complete, and persistent (23 weeks) repopulation of the CNS by peripheral myeloid cells. In repopulated mice that underwent sciatic nerve injury, we observed a normal response to mechanical stimuli, but an absence of thermal hypersensitivity ipsilateral to the injured nerve. Furthermore, we found that neuronal expression of calcitonin gene-related peptide (CGRP), which is a marker of neurons essential for heat responses, was diminished in the dorsal horn of the spinal cord in repopulated mice. These findings identify distinct mechanisms for heat and mechanical hypersensitivity and highlight a crucial contribution of CNS myeloid cells in the facilitation of noxious heat.

Keyword(s): Animals (MeSH) ; Calcitonin Gene-Related Peptide: physiology (MeSH) ; Central Nervous System: pathology (MeSH) ; Central Nervous System: physiopathology (MeSH) ; Hot Temperature (MeSH) ; Hyperalgesia: pathology (MeSH) ; Hyperalgesia: physiopathology (MeSH) ; Male (MeSH) ; Mice (MeSH) ; Mice, Inbred C57BL (MeSH) ; Mice, Transgenic (MeSH) ; Microglia: cytology (MeSH) ; Microglia: physiology (MeSH) ; Myeloid Cells: pathology (MeSH) ; Myeloid Cells: physiology (MeSH) ; Neuralgia: pathology (MeSH) ; Neuralgia: physiopathology (MeSH) ; Peptide Fragments: physiology (MeSH) ; Peripheral Nerve Injuries: pathology (MeSH) ; Peripheral Nerve Injuries: physiopathology (MeSH) ; Peripheral Nerves: pathology (MeSH) ; Peripheral Nerves: physiopathology (MeSH) ; Spinal Cord Dorsal Horn: pathology (MeSH) ; Spinal Cord Dorsal Horn: physiopathology (MeSH) ; Peptide Fragments ; calcitonin gene related peptide (1-7) ; Calcitonin Gene-Related Peptide

---

Contributing Institute(s):

1. Neuroimmunology (AG Heppner)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2018

---

Database coverage:
; ; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; DOAJ Seal ; Ebsco Academic Search ; IF >= 15 ; JCR ; SCOPUS ; Web of Science Core Collection

---