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Lactation and Prolactin Release in Foster Dams Suckling Prenatally Ethanol Exposed Pups
Author(s) -
Subramanian Marappa G.
Publication year - 1992
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1992.tb01888.x
Subject(s) - lactation , litter , prolactin , medicine , endocrinology , zoology , pregnancy , liquid diet , ethanol , gestation , biology , hormone , biochemistry , ecology , genetics
The effect of prenatal ethanol exposure on lactation was studied employing prenatally ethanol‐exposed pups transferred to foster dams following parturition. During pregnancy, from day 8 to term, dams consumed either standard laboratory chow (ad libitum control), or liquid diets containing 0%, 17.5%, or 35% ethanol derived calories (EDC). To equilize caloric intake, the 0% and 17.5% EDC groups were pair‐fed to rats in 35% EDC group. Following delivery, pups born to dams fed with laboratory chow (control) or liquid diets containing 0, 17.5, or 35% EDC were adjusted to eight per litter and transferred to foster dams, which had been fed laboratory chow and water ad libitum throughout pregnancy. Foster dams were implanted with an atrial catheter on day 3 of lactation. On days 6 (early lactation) and 10 (midlactation), following separation of litters from dams for a 6‐hr period, a baseline blood sample was removed via a catheter extension. Pups were weighed and returned to the dams. Subsequent blood samples were obtained 10, 30, 60, 120, and 180 min after initiation of suckling. Suckling latency and the amount of milk consumed during the 3‐hr suckling were also determined. Litters were weighed on days 2, 6, 10, and 21. The prolactin surge in foster dams in response to suckling by prenatally ethanol‐exposed pups was not altered on day 6 of lactation. On day 10, after the initial rise, suckling‐induced prolactin was amplified in dams suckled by prenatally ethanol‐exposed pups. This may be due to either a compensatory neuroendocrine mechanism in the foster dams for adequate milk secretion in response to the poor suckling or to the shorter but more frequent suckling episodes by prenatally ethanol‐exposed pups. On day 6 suckling latency for the 35% EDC group was greater compared to control and 17.5% EDC groups and the amount of milk consumed was lower for this group on both days 6 and 10. Pups prenatally exposed to 35% EDC diet weighed less up to weaning. These results demonstrate the continued nursing difficulty experienced by offspring and the persistence of suckling‐deficits in pups caused by prenatal ethanol exposure.