학술논문

Neuronal aromatase expression in pain processing regions of the medullary and spinal cord dorsal horn.
Document Type
article
Source
The Journal of Comparative Neurology. 525(16)
Subject
RRID:MGI:4430066
RRID:MGI:5634564
aromatase
estrogens
pain
solitary nucleus
spinal cord dorsal horn
trigeminal caudal nucleus
Afferent Pathways
Animals
Aromatase
Disease Models
Animal
Freunds Adjuvant
Gene Expression Regulation
Medulla Oblongata
Mice
Mice
Transgenic
Myelitis
Nerve Tissue Proteins
Neurons
Phosphopyruvate Hydratase
Proto-Oncogene Proteins c-fos
Sciatica
Spinal Cord Dorsal Horn
Stilbamidines
TRPV Cation Channels
Language
Abstract
In both acute and chronic pain conditions, women tend to be more sensitive than men. This sex difference may be regulated by estrogens, such as estradiol, that are synthesized in the spinal cord and brainstem and act locally to influence pain processing. To identify a potential cellular source of local estrogen, here we examined the expression of aromatase, the enzyme that catalyzes the conversion of testosterone to estradiol. Our studies focused on primary afferent neurons and on their central targets in the spinal cord and medulla as well as in the nucleus of the solitary tract, the target of nodose ganglion-derived visceral afferents. Immunohistochemical staining in an aromatase reporter mouse revealed that many neurons in laminae I and V of the spinal cord dorsal horn and caudal spinal trigeminal nucleus and in the nucleus of the solitary tract express aromatase. The great majority of these cells also express inhibitory interneuron markers. We did not find sex differences in aromatase expression and neither the pattern nor the number of neurons changed in a sciatic nerve transection model of neuropathic pain or in the Complete Freunds adjuvant model of inflammatory pain. A few aromatase neurons express Fos after cheek injection of capsaicin, formalin, or chloroquine. In total, given their location, these aromatase neurons are poised to engage nociceptive circuits, whether it is through local estrogen synthesis or inhibitory neurotransmitter release.