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  • Title: Induction of pseudopregnancy using artificial VCS: importance of lordosis intensity and prestimulus estrous cycle length.
    Author: Lehmann ML, Erskine MS.
    Journal: Horm Behav; 2004 Feb; 45(2):75-83. PubMed ID: 15019793.
    Abstract:
    In cycling female rats, vaginocervical stimulation (VCS) received naturally during mating or by artificial mechanical stimulation induces neuroendocrine and behavioral responses that are critical for reproduction, including bi-circadian prolactin surges which result in pregnancy or an 8-14-day diestrous period called pseudopregnancy (PSP). Following mating, the incidence of PSP is higher when females receive high (10) as opposed to low (3-5) numbers of intromissions. Therefore, a threshold level of VCS must be exceeded before hypothalamic changes required for PSP can occur. This study characterized the threshold curve for PSP induction for artificial VCS (VCS-a). Proestrous females were given 1, 2, 3, 4, or 8 VCS-a applied with a glass rod using 200 g of force for 2 s, with an 8-min interval between stimulations. The lordosis response (LR) to the stimulus was measured on a scale of increasing intensity from 0 to 3, and the occurrence of PSP was measured by daily vaginal lavage. In contrast to previous findings, VCS-a induced robust lordosis responses without concurrent flank and perineal stimulation. The frequency of PSP induction did not increase in females as a function of amounts of VCS-a. However, the occurrence of PSP was strongly tied to the maximum lordosis response (LR(max)) observed. PSP was observed only among multiply stimulated females that showed the highest LR(max) (3.0) to at least one of the stimulations. Multiply stimulated females that showed a LR(max) < 3.0 or females that received only one VCS-a never became PSP. PSP and a stronger LR(max) were more likely to occur in females that had 5-day compared to 4-day prestimulus estrous cycle lengths. We conclude that central mechanisms important for VCS-induced PSP and lordosis may be potentiated by estradiol's actions in estrogen-concentrating forebrain areas.
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