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The present study employed the intracranial microdialysis technique to measure norepinephrine release in the ventrolateral dendritic fields of the ventromedial hypothalamus of freely-moving animals before and during ovarian steroid (estradiol and progesterone) activation of female sexual behavior (lordosis). One day after implantation of a dialysis probe, animals were injected with 3 ,ug of estradiol benzoate followed 44 h later by 200 pg of progesterone. introduction of a male rat 4 h after progesterone treatment was correlated with dramatic increases in extracellular norepinephrine levels measured in dialysates of the ventrolateral ventromedial hypothalamus of female rats which displayed high levels of lordosis behavior. In contrast, female rats given the same steroid treatment but which did not show lordosis responses did not have elevated norepinephrine levels in their dialysates. Moreover, animals that received an estrogen antagonist concurrently with the estrogen treatment had neither an increase in ventromedial hypothalamic levels of norepinephrine during behavior testing nor did they display lordosis. These results indicate a close relationship among ovarian steroids, noradrenergic transmission in the ventromedial hypothalamus, and the expression of female sexual behavior.Lordosis is a component of female sexual behavior in rodents which is regulated by the ovarian steroids estradiol (E2) and progesterone (p) and is displayed in response to specific somatosensory stimuli (1,2). In the presence of a sexually active male rat, the complete expression of female mating behavior includes receptive (lordosis) and proceptive (darting, hopping, ear wiggling) responses. The sequential presence of E2 followed by Pis essential in that P facilitation ofestrous behavior requires prior exposure to E2 (3).It is believed that E2 and P exert their facilitatory effects on lordosis by acting on target neurons in the ventromedial nucleus of the hypothalamus (VMN) (4). The ventrolateral dendriticfields of these neurons are densely innervated by norepinephrine (NE) neurons originating in the brainstem (5, 6). Moreover, lesions which eliminate the NE input to the hypothalamus also abolish hormone-facilitated lordosis behavior in female rats (7,8). Thus, we have hypothesized that E2 and P regulation of female mating behavior may be mediated in part by augmentation of NE transmission in the ventromedial hypothalamus (VMH). This hypothesis was supported by our previous study employing intracranial microdialysis of the ventrolateral VMH in urethaneanesthetized female rats (9). We demonstrated that combined treatment with E2 and P. but neither E2 nor P alone, enhances KCI-evoked N E release in the ventrolateral VMH. To investigate further the hypothesis that E2 and P modulate NE release in the VMH, and to assess the possible role of this modulation in lordosis behavior, the present experiments measured NE release in the ventrolateral VMH of freely-moving animals using the microdialysis technique.Results Fig. 1 shows a repre...

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