Control of Hypothalamic Tyrosine Hydroxylase

Arbogast, Lydia A.

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
• Type: Research Project (R01)
• Project #: 1R01HD035332-01
• Application #: 2208252
• Study Section: Biochemical Endocrinology Study Section (BCE)
• Project Start: 1996-09-01
• Project End: 1999-08-31
• Budget Start: 1996-09-01
• Budget End: 1997-08-31
• Support Year: 1
• Fiscal Year: 1996

Institution

• Name: Southern Illinois University Carbondale
• Department: Physiology
• Type: Schools of Medicine
• DUNS #: 939007555
• City: Carbondale
• State: IL
• Country: United States
• Zip Code: 62901

Publications

Arbogast, Lydia A; Voogt, James L (2002) Progesterone induces dephosphorylation and inactivation of tyrosine hydroxylase in rat hypothalamic dopaminergic neurons. Neuroendocrinology 75:273-81

Arbogast, L A (2001) Calmodulin and a cyclic nucleotide-dependent protein kinase facilitate the prolactin-induced increase in tyrosine hydroxylase activity in tuberoinfundibular dopaminergic neurons. Endocrine 16:105-12

Arbogast, L A; Hyde, J F (2000) Estradiol attenuates the forskolin-induced increase in hypothalamic tyrosine hydroxylase activity. Neuroendocrinology 71:219-27

Arbogast, L A; Shah, G V; Voogt, J L (1999) 3,5 cyclic adenosine monophosphate mediates the salmon calcitonin-induced increase in hypothalamic tyrosine hydroxylase activity. Endocrinology 140:3273-81

Arbogast, L A; Voogt, J L (1997) Prolactin (PRL) receptors are colocalized in dopaminergic neurons in fetal hypothalamic cell cultures: effect of PRL on tyrosine hydroxylase activity. Endocrinology 138:3016-23