Behavioral, Reproductive &amp; Neuroendocrine Consequences of   Prenatal Stress
{'Code': '08090200', 'Directorate': {'Abbreviation': 'BIO', 'LongName': 'Direct For Biological Sciences'}, 'Division': {'Abbreviation': 'IOS', 'LongName': 'Division Of Integrative Organismal Systems'}}
{'SignBlockName': 'Fred Stollnitz', 'PO_EMAI': None, 'PO_PHON': None}
Female mammals, particularly rodents, exhibit a number of reproductive          deficits as a consequence of exposure to prenatal stress.  Among the            most serious are the effects upon fertility and fecundity.  To date,            there has not been a systematic analysis that has delineated those              factors responsible for the deficits on reproductive physiology and             possibly behavior in prenatally stressed females.  In the present               proposal the reproductive deficits present in the prenatally-stressed           female will be studied with focus upon physiological, i.e.                      endocrine/neuroendocrine, and behavioral processes and the interactions         between the behavioral state of the female and her physiological                responses.  In preliminary studies, decrements in reproductive success          in prenatally-stressed female rats were found with as many as 80% of            these females failing to carry their pregnancies to term and only 10% of        the mated females raising a litter through the first week of lactation.         In addition, prenatally-stressed females were behaviorally less                 responsive to their young, and prenatally-stressed females showed               diminished endocrine responses as adults.  Since both pregnancy                 maintenance as well as the induction of maternal behavior in the rat are        under endocrine (hormonal) control, it is possible that the deficits in         pregnancy maintenance, lactational performance, and maternal behavior in        the prenatally-stressed female, may result from a common underlying             deficiency in the female's ability to secrete hormones, a deficiency            brought about by exposure to stress in utero.  In the current research,         Drs. Robert Bridges and Craig Kinsley are studying the potential common         underlying physiological mechanisms that contribute to both the                 decrements in reproductive physiology and behavior.  The work will focus        on whether the detriments in pregnancy, lactation and behavior result           from changes in hormone (prolactin) regulation and action brought about         by the prenatal stress experience.  The results of these studies will           help to define those factors responsible for the normal maintenance of          pregnancy and lactation, and will provide a data base for evaluating            analogous endocrine and behavioral deficits in other mammals, including         humans.
[{'FirstName': 'Robert', 'LastName': 'Bridges', 'PI_MID_INIT': 'S', 'PI_SUFX_NAME': None, 'PI_FULL_NAME': 'Robert S Bridges', 'EmailAddress': 'RBRIDGES@OPAL.TUFTS.EDU                 5088397091', 'NSF_ID': '000206688', 'StartDate': '08/15/1987', 'EndDate': None, 'RoleCode': 'Principal Investigator'}, {'FirstName': 'Craig', 'LastName': 'Kinsley', 'PI_MID_INIT': 'H', 'PI_SUFX_NAME': None, 'PI_FULL_NAME': 'Craig H Kinsley', 'EmailAddress': 'ckinsley@richmond.edu', 'NSF_ID': '000464072', 'StartDate': '08/15/1987', 'EndDate': None, 'RoleCode': 'Co-Principal Investigator'}]
{'Name': 'Harvard University', 'CityName': 'CAMBRIDGE', 'ZipCode': '021385366', 'PhoneNumber': '6174955501', 'StreetAddress': '1033 MASSACHUSETTS AVE STE 3', 'StreetAddress2': None, 'CountryName': 'United States', 'StateName': 'Massachusetts', 'StateCode': 'MA', 'CONGRESSDISTRICT': '05', 'CONGRESS_DISTRICT_ORG': 'MA05', 'ORG_UEI_NUM': 'LN53LCFJFL45', 'ORG_LGL_BUS_NAME': 'PRESIDENT AND FELLOWS OF HARVARD COLLEGE', 'ORG_PRNT_UEI_NUM': None}
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{'Code': '1160', 'Text': 'IBN ANIMAL BEHAVIOR'}
{'url': 'https://www.nsf.gov/awardsearch/download?DownloadFileName=1987&All=true', 'xml': '8708330.xml'}