Lesions in the midbrain dorsal central gray (MCGL) markedly suppressed both lordosis and soliciting behavior in estradiol benzoate-progesterone (EB-P)-primed castrated female rats. Similarly, the pontine dorsomedial tegmental lesions (PDMTL) caused a severe loss of lordosis behavior. However, the PDMTL females while demonstrating no lordotic response displayed ear-wiggling. These results suggest that the midbrain dorsal central gray plays an important role in regulation of both lordosis and soliciting behaviors. In contrast, the pontine dorsomedial tegmentum appears to participate in regulating the neural mechanism for lordosis only and not for soliciting behavior. Two weeks later prior to a second test, approximately half of the MCGL and PDMTL females that had shown no lordosis in the first test, were injected with p-chlorophenylalanine (PCPA) and primed with EB-P. PCPA significantly increased the lordotic activity of EB-P-primed MCGL females, whereas it failed to potentiate a lordotic response in the PDMTL females. Since PCPA effectively facilitated the display of lordosis in the absence of the neural substrate of the midbrain central gray, this neural structure may not be the minimally necessary component of the neural circuitry regulating the display of lordosis behavior. On the other hand, the pontine dorsomedial tegmentum may be a neural substrate more closely related with the descending pathway controlling the expression of lordosis.
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