The effects of transection of fiber connections with the medial basal hypothalamus (MBH) on induction or maintenance of pseudopregnancy (PSP) were studied. PSP was induced 'pharmacologically' by injecting reserpine (1 mg/kg) on the day of diestrus I in 4-day cycling rats or the corresponding day after induction of ovulation in persistent estrous animals. Postero-bilateral deafferentation (PBLD) which cuts dorsal, lateral and posterior connections to the MBH failed to influence the induction of PSP. All rats resulted in PSP following reserpine injection. Anterior deafferentation (AD) which interrupts the preoptic-hypothalamic connections induced anovulatory persistent vaginal estrus. In these AD rats, reserpine could not activate new corpora lutea which had been formed by a pretreatment with 10 I.U. HCG. However, replacement therapy with 20 I.U. prolactin was successful in activating these corpora lutea. In spite of the AD, all rats thereafter remained in diestrus, massive deciduomata being formed following uterine trauma. In the second series of experiments, the AD or roof deafferentation (RD) was performed 3 days after reserpine injection. The AD effectively interrupted reserpine-induced PSP. However, this effect of the AD was reversed by the replacement with prolactin from the day of operation. PSP was also not interrupted by the AD when reserpine was given supplementarily from the day of the AD through the day before autopsy, but a single dose of reserpine only on the day of the AD was not effective in maintaining PSP in AD rats. The RD which removes dorsal afferents to the preoptic area (POA) and hypothalamus did not interfere with PSP; it continued in all rats of the group. These results suggest that neural influence originating from the POA or more rostral regions is necessary to maintain prolonged release of prolactin during PSP. Since successive injections of reserpine were needed to keep the AD rats pseudopregnant, reserpine sensitive neural structures which may locate behind the surgical cut seem to be unable to support independently prolonged release of prolactin during PSP.
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