Central
pain syndrome is characterized by severe and excruciating
pain resulting from a lesion in the central nervous system. Previous studies have shown that
estradiol decreases
pain and that inhibitors of the
enzyme aromatase, which synthesizes
estradiol from aromatizable
androgens, increases
pain sensitivity. In this study we have assessed whether
aromatase expression in the dorsal horns of the spinal cord is altered in a rat model of central
pain syndrome, induced by the unilateral electrolytic lesion of the spinothalamic tract.
Protein and
mRNA levels of
aromatase, as well as the
protein and
mRNA levels of
estrogen receptors α and β, were increased in the dorsal horn of female rats after spinothalamic tract injury, suggesting that the injury increased
estradiol synthesis and signaling in the dorsal horn. To determine whether the increased
aromatase expression in this
pain model may participate in the control of
pain,
mechanical allodynia thresholds were determined in both hind paws after the intrathecal administration of
letrozole, an
aromatase inhibitor.
Aromatase inhibition enhanced
mechanical allodynia in both hind paws. Because
estradiol is known to regulate
gliosis we assessed whether the spinothalamic tract injury and
aromatase inhibition regulated
gliosis in the dorsal horn. The proportion of microglia with a reactive phenotype and the number of
glial fibrillary acidic protein-immunoreactive astrocytes were increased by the injury in the dorsal horn.
Aromatase inhibition enhanced the effect of the injury on
gliosis. Furthermore, a significant a positive correlation of
mechanical allodynia and
gliosis in the dorsal horn was detected. These findings suggest that
aromatase is up-regulated in the dorsal horn in a model of central
pain syndrome and that
aromatase activity in the spinal cord reduces
mechanical allodynia by controlling reactive
gliosis in the dorsal horn.