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Reproductive Neuroendocrinology
My laboratory is interested in how female reproductive hormones affect neuronal activity in the brain. The overall goal is to
understand the control of prolactin secretion during lactation and the female reproductive cycle. A primary focus is cellular
and molecular mechanisms involved in the regulation of dopamine and opioid peptide neurons, particularly as related to feedback to the
hypothalamus by prolactin from pituitary gland and steroid hormones, estradiol and progesterone, from the ovary. Integrative, cell
culture and molecular biology approaches are used to
identify cell signaling pathways and transcriptional and post-translational control of key enzymes in neurotransmitter biosynthesis.
Recent Publications:
Arbogast LA, Hyde, JF. Estradiol attenuates the forskolin-induced increase in hypothalamic tyrosine hydroxylase activity. Neuroendocrinology 71:219-227,2000.
Arbogast LA. Calmodulin and a cyclic nucleotide protein kinase facilitate the prolactin-induced increase in tyrosine hydroxylase activity in tuberoinfundibular dopaminergic neurons. Endocrine 16:105-112, 2001.
Arbogast LA, Voogt JL. Progesterone induces dephosphorylation and inactivation of tyrosine hydroxylase in hypothalamic dopaminergic neurons. Neuroendocrinology 75:273-281, 2002.
Nahi F, Arbogast LA. Prolactin modulates hypothalamic preproenkephalin, but not proopiomelanocortin, gene expression during lactation. Endocrine 20:115-122, 2003.
Liu B, Arbogast LA. Phosphorylation state of tyrosine hydroxylase in the stalk-median eminence is decreased by progesterone in cycling female rats. Endocrinology 149:1462-1469, 2008 PMID: 18096660 |
