REPRODUCTIVE BEHAVIOR 



1231 



fornix or amygdala-piriform-cortex appeared to mate 

 normally, but not in a hypersexual manner, and to 

 ovulate in response to such mating (78). 



Diencephalic and Hypothalamic Mechanisms 



The mechanisms discussed above have pointed to 

 the diencephalon as the site of 'higher centers' with 

 reference to the cord and lower brain stem, and 'sub- 

 cortical centers' with reference to the cerebrum. Since 

 integrated estrous behavior can be evoked in the 

 absence of the cereisrum but not in animals with brain- 

 stem transection below the midbrain, the highest es- 

 sential center for estrous behavior would appear to 

 lie between the rostral midbrain and the preoptic 

 region. 



Large thalamic lesions in connection with cerebral 

 damage did not eliminate sexual behavior in the fe- 

 male cat (5). Dempsey and Morison [discussed in 

 Beach (12)] removed the thalamus bilaterally in cats 

 that later mated, maintained pregnancy and deiixcred 

 young but failed to care properly for them. Large 

 thalamic lesions did not prevent mating or ovulation 

 in the rabbit, according to Sawyer (unpublished ob- 

 servations). 



Among the earlier hypothalmic lesions with a bear- 

 ing on the problem were those of Ranson (71) who 

 reported that female cats with tuberal lesions behind 

 the infundiinilum mated and gave birtii to litters. 

 Later work in Ranson's laboratory (31) showed that 

 female cats with lesions in the anterior hypothalamus 

 around the supraoptic nuclei did not mate. This was 

 confirmed by Dey el al. (23), and Brookliart el al. 

 (16, 17) showed that estrogen treatment would not 

 induce receptivity in guinea pigs with anterior hypo- 

 thalamic lesions. Maes (62) demonstrated that in es- 

 trogen-treated female cats the pituitary gland was un- 

 necessary for apparently complete mating behavior. 



An observation of considerable influence was made 

 in 1939; Dempsey & Rioch reported (22) that brain- 

 stem transection rostral to the mammillary bodies 

 was consistent with mating while similar section be- 

 hind the mammillary bodies resulted in anestrus. 

 Actually the definite results were obtained with one 

 guinea pig and one cat. In the light of these findings 

 Bard (6) interpreted the hypothalamic lesions of 

 Magoun and Bard as indicating that the highest cen- 

 ter of sex behavior in the cat lay in the rostral mesen- 

 cephalon. However, as indicated below, the evidence 

 of Magoun and Bard is consistent with the presence 

 of a sex center in the anterior hypothalamus. 



Sawyer & Robison (81) have recently found in 



FIG. 4. Base of the cat brain showing the area in piriform 

 cortex [solid black) in which lesions most consistently induced 

 hypersexuality in males. [From Green et al. (41).] 



female cats that anterior hypothalamic lesions rostral 

 to the ventromedial nuclei and either medial to or 

 within the area of the medial forebrain bundle result 

 in permanent anestrus in 1 1 out of 14 cases in spite of 

 treatment with exogenous estrogen. Such lesions do 

 not interfere with tlie trophic influence of the hypo- 

 physis on the ovary, and ovulation can be induced by 

 direct electrical stimulation of the ventromedial 

 nucleus. Lesions in the ventromedial nucleus, the 

 premammillary region or tho.se entirely destroying 

 the mammillary body result in anestrus due to ovarian 

 atrophy from pituitary hypofunction. However, if 

 such cats are supplied with exogenous estrogen, they 

 show all the usual behavioral responses of mating 

 and after-reaction. Typical lesions are illustrated in 

 figure 5. The results confirm the findings of Ranson's 

 laboratory and do not support the work of Dempsey & 

 Rioch (22) in the cat. Bard's (6) figures reveal de- 

 struction of the anterior region in a cat which would 

 not mate and the sparing of this region in a lesion- 

 bearing cat that subsequenty became receptive on 

 estrogen treatment. 



