TY - JOUR
T1 - 17β-estradiol regulation of the mRNA expression of T-type calcium channel subunits
T2 - Role of estrogen receptor α and estrogen receptor β
AU - Bosch, Martha A.
AU - Hou, Jingwen
AU - Fang, Yuan
AU - Kelly, Martin J.
AU - Rønnekleiv, Oline K.
PY - 2009/1/20
Y1 - 2009/1/20
N2 - Low-voltage-activated (T-type) calcium channels are responsible for burst firing and transmitter release in neurons and are important for exocytosis and hormone secretion in pituatary cells. T-type channels contain an α1 subunit, of which there are three subtypes, Cav3.1, -3.2, and -3.3, and each subtype has distinct kinetic characteristics. Although 17β-estradiol (E2) modulate T-type calcium channel expression and function, little is known about the molecular mechanisms involved. We used real-time PCR quantification of RNA extracted from hypothalamic nuclei and pituitary in vehicle and E2-treated C57BL/6 mice to elucidate E2-mediated, regulation of Cav3.1, -3.2, and -3.3 subunits. The three subunitis expressed in both the hypothalamus and the pituitary. E2 treatment increased the mRNA expression of Cav3.1 and -3.2, but not Cav3.3, in the medial preotic are and the arcuate nucleus. In the pituitary, Cav3.1 was increased with E2 treatment, and Cav3.2 and -3.3 were decreased. To examine whether the classical estrogen receptors (ERs) were involved in the regulation, we used ERα- and ERβ-deficient C57BL/6 mice and explored the effects of E2 on T-type channel subtypes. Indeed, we found that the E2-induced increase in Cav3.1 in the hypothalamus was dependent on ERα whereas the E2 effect on Cav3.2 was dependent on both ERα and ERβ. However, the E2-induced effects in the pituitary were dependent on only the expression of ERα. The robust E2 regulation of T-type calcium channels could be an important mechanism by which E2 increases the excitability of hypothalamic neurons and modulates pituitary secretion.
AB - Low-voltage-activated (T-type) calcium channels are responsible for burst firing and transmitter release in neurons and are important for exocytosis and hormone secretion in pituatary cells. T-type channels contain an α1 subunit, of which there are three subtypes, Cav3.1, -3.2, and -3.3, and each subtype has distinct kinetic characteristics. Although 17β-estradiol (E2) modulate T-type calcium channel expression and function, little is known about the molecular mechanisms involved. We used real-time PCR quantification of RNA extracted from hypothalamic nuclei and pituitary in vehicle and E2-treated C57BL/6 mice to elucidate E2-mediated, regulation of Cav3.1, -3.2, and -3.3 subunits. The three subunitis expressed in both the hypothalamus and the pituitary. E2 treatment increased the mRNA expression of Cav3.1 and -3.2, but not Cav3.3, in the medial preotic are and the arcuate nucleus. In the pituitary, Cav3.1 was increased with E2 treatment, and Cav3.2 and -3.3 were decreased. To examine whether the classical estrogen receptors (ERs) were involved in the regulation, we used ERα- and ERβ-deficient C57BL/6 mice and explored the effects of E2 on T-type channel subtypes. Indeed, we found that the E2-induced increase in Cav3.1 in the hypothalamus was dependent on ERα whereas the E2 effect on Cav3.2 was dependent on both ERα and ERβ. However, the E2-induced effects in the pituitary were dependent on only the expression of ERα. The robust E2 regulation of T-type calcium channels could be an important mechanism by which E2 increases the excitability of hypothalamic neurons and modulates pituitary secretion.
KW - Cav3.1
KW - Cav3.2
KW - Cav3.3
KW - Hypothalamus
KW - Pituitary
KW - α1 subunits
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U2 - 10.1002/cne.21901
DO - 10.1002/cne.21901
M3 - Article
C2 - 19003958
AN - SCOPUS:59149097032
SN - 0021-9967
VL - 512
SP - 347
EP - 358
JO - Journal of Comparative Neurology
JF - Journal of Comparative Neurology
IS - 3
ER -