Abstract
The data summarized here suggest the existence of a new central pathway for the hormonal regulation of pain. These data mainly collected in quail, a useful model in neuroendocrinology, demonstrate that numerous neurons in the superficial laminae of the spinal cord express aromatase (estrogen-synthase). Chronic and systemic blockade of this enzyme in quail alters nociception within days, indicating that the slow genomic effects of sex steroids on nociception classically observed in mammals also occur in birds and require aromatization of androgens into estrogens. However, by contrast with these slow effects, acute intrathecal inhibition of aromatase in restricted spinal cord segments reveals that estrogens can also control nociception much faster, within 1 min, presumably through the activation of a nongenomic pathway and in a manner that depends on an immediate response to fast activation/deactivation of local aromatase activity. This emergent central and rapid paracrine mechanism might permit instantaneous and segment-specific changes in pain sensitivity; it draws new interesting perspectives for the study of the estrogenic control of pain, thus far limited to the classical view of slow genomic changes in pain, depending on peripheral estrogens. The expression of aromatase in the spinal cord in other species and in other central nociception-related areas is also briefly discussed.
