LH release and ovulation in the rat following depletion of hypothalamic norepinephrine: chronic vs. acute effects

The effects of long-term hypothalamic norepinephrine (NE) depletion on reproductive cyclicity, ovulation, and luteinizing hormone (LH) release were studied in adult female rats. Bilateral transections of the ascending noradrenergic pathway (ANP) at the level of the mesencephalon led to an 83% depletion of hypothalamic NE. Although some animals exhibited a period of acyclicity following this surgical procedure, by 23 days all animals had begun to cycle. When checked for ovulation at around 40 days, all of the rats had shed full quotas of ova. There was no significant difference in either the timing or magnitude of the surge when proestrous LH levels in NE-depleted rats were compared with sham transected controls. To see if the residual hypothalamic NE left after transection of the ascending noradrenergic pathway was important for maintenance of normal LH secretion and ovulation, a group of long-term depleted rats were given an NE synthesis inhibitor (diethyldithiocarbamate: DDC). In all of the sham-cut and intact control rats this drug either partially or completely blocked ovulation, but it was effective in only 40% of the depleted animals. The other 60% not only ovulated, but shed full quotas of ova. These results demonstrate that normal LH secretion can occur even when hyplthalamic NE levels are extremely low. Although acute depressions of NE by pharmacological agents such as DDC effectively block the LH surge, this inhibition is not sustained when NE is depleted over long periods of time. Therefore, NE apparently plays a modulatory, rather than mandatory, role in control of LH release and ovulation.