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The Effects of Glutamate on Oxytocin Release
Author(s) -
Badmus Yetunde Awwah,
Cantley Richard,
Hill Jennifer W
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1038.7
Subject(s) - glutamatergic , lactation , oxytocin , endocrinology , medicine , glutamate receptor , biology , prolactin , hormone , offspring , pregnancy , genetics , receptor
During pregnancy, weight gain creates a positive energy balance that serves the biological purpose of providing adequate energy stores for the upcoming extended period of lactation. However, excess adiposity is associated with a delay in the initiation of lactation and a reduced duration of breastfeeding. Glutamatergic neurons in the paraventricular nucleus (PVN) are implicated in the control of oxytocin release. Recent studies have also shown that glutamatergic target neurons in this nucleus mediate much of the ability of melanocortins to suppress feeding. Based on novel preliminary data, we hypothesize that glutamatergic neurons of the PVN influence prenatal and postnatal hyperphagia and modify the activity of oxytocin neurons involved in lactation. To test this hypothesis, we have created vglut2/sim1‐cre female mouse, in which the gene for the vesicular glutamate transporter VGLUT2 has been deleted in the PVN. To examine dysfunctional lactation in this model we evaluated multiple parameters including neonatal survival and growth, and analysis of mammary tissue and ovary tissue. In addition, circulating oxytocin, prolactin, and other hormone levels were measured. The number of pups born to homozygous vglut2/sim1 dams that survive until weaning was dramatically down compared to controls; 0% survival was observed when fostering did not occur compared to approximately 100% survival when fostering did occur. Results to date suggest that homozygous vglut2/sim1 mice show a consistent and complete deficit in milk release and a buildup of milk protein and lipids within the mammary glands. In addition, we have observed a potential subfertility phenotype observed in the vglut2/sim1 females. These results highlight a potential pathway whereby obesity and lactational deficiency may develop concurrently. Additional studies will be needed to test whether the glutamatergic neuronal populations in the PVN controlling body weight and lactation overlap. Support or Funding Information Supported by a Michigan Diabetes Research and Training Center Pilot & Feasibility Study Grant (P30DK092926:5556) to JWH.