GnRH in the spinal subarachnoid space potentiates lordosis behavior in the female rat

Abstract

Gonadotropin releasing hormone (GnRH) (100 ng) infused directly into the spinal subarachnoid space via a chronically implanted catheter, induced a prompt facilitation of lordosis behavior in estrogen-primed ovariectomized female rats. Facilitation occurred within 5 min and lasted for 3 1/2 hr. This effect of GnRH could be blocked by a GnRH antagonist analog, [D-Phe2, Pro3, D-Phe6] GnRH (250 ng) which also completely abolished lordosis within 2 1/2 hr. The antagonist analog (250 ng) but not a high titre specific anti-GnRH antiserum (enough to neutralize 24 micrograms of GnRH) abolished lordosis when infused alone in the subarachnoid space in estrogen-primed rats. The antagonist but not the anti-GnRH antiserum also significantly suppressed lordosis in estrogen-progesterone primed female rats. Supporting experiments showed that the effects of GnRH and its antagonist may not be due to their effects on supraspinal structures by diffusion from the spinal subarachnoid space. These results may indicate a direct effect of GnRH and its antagonist at the level of the spinal cord and may suggest a possible role for GnRH in the processing of somatosensory information necessary for the trigger of lordosis.