Sexually dimorphic areas in the rat medial amygdala: resistance to the demasculinizing effect of prenatal stress.

Exposure to prenatal stress blocks full masculinization of several sexually dimorphic nuclei in the brain and spinal cord of male rats. We now compare the adult volume of the medical amygdala (MA) and two of its component cell groups, posterodorsal (MePD) and posteroventral (MePV), in prenatally stressed male rats and nonstressed males and females. Previous reports of sex differences (male > female) in the overall size of the MA and the MePD component were confirmed, and we identified a previously unreported sex difference (male > female) in MePV. Prenatal stress had no effect on the size of the total MA, or of the MePD or MePV in males. Maternal stress attenuates the surge in plasma testosterone (T) which normally occurs on days 18 and 19 of gestation in male rats. This brief suppression of T during prenatal development leads to incomplete masculinization of some sexually dimorphic features of the CNS (i.e. the SDN-MPOA of the hypothalamus, and SNB and DLN of the spinal cord) but not others (i.e. the MA, MePD, and MePV). The selective effects of prenatal stress on neural differentiation may be due to differences in the onset and duration of the periods when each of these structures in most sensitive to T and/or its metabolites.

Facilitation of sexual receptivity by hypothalamic and midbrain implants of progesterone in female hamsters.

In the first experiment, ovariectomized female hamsters were stereotaxically implanted with bilateral guide cannulae aimed at the medial preoptic area (POA), ventromedial hypothalamus (VMH), or ventral tegmentum (VTA). The following week these females were injected SC with 10 micrograms estradiol benzoate (EB) and then had 27-gauge cannulae containing crystalline progesterone inserted through the guide tubes. Sexual receptivity was observed in 3 of 11 animals with VMH implants of progesterone, in 2 of 10 with VTA progesterone, but in none with POA implants. In the second experiment, the amount of intracranial progesterone was increased by mechanically expelling a 1.5 micrograms progesterone pellet from the tip of each cannula insert. This treatment facilitated receptivity in 10 of 20 hamsters with VTA implants and in 9 of 32 VMH-implanted animals. This induction of receptivity required approximately 2 hr. Progesterone pellets in the POA, mammillary region, and lateral mesencephalon were generally ineffective. In hamsters, progesterone into either the VMH or the VTA is sufficient to facilitate receptivity, although neither site is highly sensitive to progesterone. These results differ from those in recent studies in rats and this difference may reflect important species differences in the control of lordosis.

Sexual receptivity: brain sites of estrogen action in female hamsters.

In order to investigate the brain sites of estrogen action, ovariectomized hamsters were stereotaxically implanted with unilateral 27 gauge cannulae containing estradiol. Groups of females received implants into either the lateral septum, bed nucleus of the stria terminalis, preoptic area, anterior hypothalamus, ventromedial hypothalamus, arcuate nucleus, corticomedial amygdala or mesencephalic central gray. Another set of animals received implants containing cholesterol. One week later the animals were injected with progesterone and 4-5 hours later tested for sexual receptivity. The most receptivity and the most consistent response was seen in females with estradiol implants in the ventromedial hypothalamus. Only a few scattered animals in the other anatomical groups showed any receptivity. Only in animals with implants in the anterior hypothalamus was there any evidence of leakage of estrogen into peripheral circulation as measured by uterine weight. There was no response in females with cholesterol implants. Our results suggest that the ventromedial hypothalamus is the most sensitive brain area for the estrogenic induction of female sexual receptivity in hamsters.

Sagittal knife cuts in the near and far lateral preoptic area-hypothalamus disrupt maternal behaviour in female hamsters.

Parasagittal knife cuts with a varied mediolateral position were placed along the medial preoptic-medial anterior hypothalamic continuum (MPOA-MAH) in female hamsters. Near lateral (NL) knife cuts severed mediolateral connections between the MPOA-MAH and the medial forebrain bundle (MFB) while far lateral cuts (FL) were placed more laterally, sparing MPOA-MAH connections with the MFB. Across the knife cut condition, hamsters were either allowed to construct and maintain a food hoard or allowed to feed ad lib but not permitted to hoard. Animals were then tested for maternal behaviours. Both NL and FL cuts disrupted pup-directed behaviours in virgin maternal tests. NL, but not FL cuts severely disrupted nest building. These same animals were then mated and tested for maternal behaviour with their own young. There were no differences among the experimental groups in various maternal behaviours during these tests. Throughout lactation, however, the majority of NL and FL hamsters not permitted to hoard progressively cannibalized their entire litters. NL and FL counterparts with the hoarding opportunity, on the other hand, cannibalized fewer pups and reared healthy, moderate-sized litters that were smaller than those of surgical controls. That FL cuts were just as effective as NL cuts in disrupting pup-directed behaviour suggests that the mediolateral connections of the MPOA-MAH, other than with the MFB, are important for these behaviours.

Suppression of sexual receptivity in the female hamster: neuroanatomical projections from preoptic and anterior hypothalamic electrode sites.

Electrical stimulation (ES) through fine-wire electrodes chronically implanted in the preoptic area and anterior hypothalamus suppressed the lordosis response in freely moving hormone-primed female hamsters. ES at these sites never induced or facilitated lordosis. When behavioral testing was completed small lesions were made at the tips of the electrodes, and the Fink-Heimer method was used to trace degenerating axons away from the sites of ES. This was done in an effort to determine the neural pathways important for the modulation of this behavior. The hypothalamic distribution of the stria terminalis was also charted for the hamster and was found to be similar to that in the rat, including projections to both the shell and core of the ventromedial nucleus (VMN). No single pattern of degeneration was common to all females showing ES-produced lordosis suppression. These data demonstrate that stimulation of several different pathways can produce behavioral states that are incompatible with the lordosis response. We suggest that ES in the medial preoptic-medial anterior hypothalamic continuum suppresses sexual receptivity by influencing neurons in the VMN region, while ES through more laterally placed electrodes suppresses receptivity by producing an incompatible state of behavioral activation, without directly influencing VMN region neural activity.

Sagittal knife cuts in the far-lateral hypothalamus reduce sexual receptivity in female hamsters.

We have previously shown that hypothalamic knife cuts confined to the sagittal plane lateral to the medial anterior hypothalamus-ventromedial nucleus can disrupt sexual receptivity in female golden hamsters. In the present study we have compared the effects of varying the lateral position of sagittal cuts located at this same rostral-caudal level. Near-lateral (NL) cuts were placed at or just lateral to the fornix, while far-lateral (FL) cuts were placed at the lateral edge of the medial forebrain bundle. Ovariectomized, estradiol benzoate plus progesterone-treated females were given weekly tests for lordosis before and after hypothalamic cuts. Changes in body weight and agonistic behavior were also recorded. Both NL and FL cuts reduced lordosis in response to both manual stimulation and a sexually active male. Postoperatively, it was more difficult to elicit lordosis from these females, and if elicited, the duration of the response was reduced. NL, but not FL, cuts also increased agonistic behavior, and produced obesity. Since both NL and FL cuts severed axons traveling in the region of the supraoptic commissures (SOC), these data support our hypothesis that these SOC connections are critical for sexual receptivity. The SOC carrys both efferents and afferents of the ventromedial hypothalamus. Sagittal-plane cuts which interrupt the SOC may disrupt lordosis by cutting either or both types of connection.