Kirby showed that acutely stressed rats showed increased RFRP levels for several hours, but that levels returned to normal by the next day. Chronically stressed rats, however, were left with longer-term elevations of RFRP levels in the dorsomedial hypothalamus area of the brain, and suppression of activity in the reproductive axis - the hypothalamus-pituitary-gonadal hormone cascade - that is associated with lowered sexual activity.
"With chronic stress, glucocorticoids went sky high," Kirby said.
To determine the role of glucocorticoids, Kirby removed the adrenal glands of male rats, eliminating the source of the hormone. Without adrenals, stress no longer affected RFRP levels in the brain. The researchers also showed that the cells that produce RFRP have receptors for glucocorticoids, a clear indication that these stress hormones can directly affect the cells that produce RFRP.
"Critically, we show that RFRP neurons express the receptors for glucocorticoids, which are released from the adrenal glands in response to stress, and that removal of the adrenal glands prevents the stress-induced, up-regulation of RFRP," Bentley said. "Thus, we believe we have identified an entirely novel pathway for stress-induced reproductive dysfunction."
Kirby noted that adrenal hormones are critical to survival, so removing the gland and thus glucocorticoids is not a solution to chronic stress.
However, Kaufer said, it may be possible to block GnIH to reduce some of the effects of stress on reproduction.
The researchers plan to confirm the results in female rats and investigate further the role of GnIH in reproduction.
|Contact: Robert Sanders|
University of California - Berkeley