Modulation of olfactory bulb tyrosine hydroxylase and catecholamine transporter mRNA by estrogen.
Since estrogen exerts wide ranging effects within the central nervous system, it is important to investigate the sites and actions of this gonadal steroid hormone at extra-hypothalamic locations. In the present report, the effects of estrogen upon catecholaminergic function within the olfactory bulb were examined. To assess the role of estrogen at this site, ovariectomized mice received either no further hormonal treatment or were treated with estrogen, the anti-estrogen, tamoxifen, or a combination of estrogen and tamoxifen as administered in a 21-day release pellet. At 14 days post-hormonal treatment, the olfactory bulbs were assayed for mRNA levels of tyrosine hydroxylase, dopamine transporter and norepinephrine transporter using competitive-PCR. Tyrosine hydroxylase mRNA levels in either estrogen or estrogen+tamoxifen treated females were significantly decreased compared with non-hormonally treated controls. In addition, tyrosine hydroxylase mRNA levels of tamoxifen-treated mice were significantly greater than that of estrogen-treated mice. Dopamine transporter mRNA levels of tamoxifen-treated females were significantly greater than that of non-hormonally treated controls and estrogen treated mice. The combination of estrogen+tamoxifen significantly increased dopamine transporter mRNA levels compared to that of estrogen treated mice. No overall statistically significant differences in norepinephrine transporter mRNA levels were obtained among the four treatment groups. The data demonstrate that estrogen can exert significant modulatory effects upon olfactory bulb catecholaminergic function. Therefore, events which alter estrogen levels (menstrual/estrogen cycle, pregnancy/lactation, menopause, tamoxifen treatment) can modulate olfactory bulb catecholaminergic functions which may be involved with the detection and processing of olfactory stimuli.
Dluzen
Dean E
DE
Department of Anatomy, Northeastern Ohio Universities College of Medicine (NEOUCOM), 4209 State Route 44, PO Box 95, Rootstown 44272-0095, USA. ded@neoucom.edu
Park
June-Hee
JH
Kim
Kyungjin
K
D000818:Animals; D003692:Delayed-Action Preparations; D050483:Dopamine Plasma Membrane Transport Proteins; D004338:Drug Combinations; D004965:Estrogen Antagonists / Q000008:administration & dosage; D004967:Estrogens / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins / Q000235:genetics* / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D008969:Molecular Sequence Data; D009419:Nerve Tissue Proteins; D050484:Norepinephrine Plasma Membrane Transport Proteins; D009830:Olfactory Bulb / Q000187:drug effects* / Q000201:enzymology / Q000502:physiology*; D010052:Ovariectomy; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D027981:Symporters / Q000235:genetics* / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000235:genetics* / Q000378:metabolism
D003692:Delayed-Action Preparations; D050483:Dopamine Plasma Membrane Transport Proteins; D004338:Drug Combinations; D004965:Estrogen Antagonists; D004967:Estrogens; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins; D009419:Nerve Tissue Proteins; D050484:Norepinephrine Plasma Membrane Transport Proteins; D012333:RNA, Messenger; C493228:Slc6a2 protein, mouse; C493226:Slc6a2 protein, rat; D027981:Symporters; D014446:Tyrosine 3-Monooxygenase