Membrane Effects of Thyrotropin-Releasing Hormone and Estrogen Shown by Intracellular Recording from Pituitary Cells

Abstract

The effects of thyrotropin-releasing hormone and 17 β-estradiol on the electrical membrane properties of a prolactin-secreting pituitary cell line (GH 3 /B6) were studied with intracellular microelectrode recordings. Of the cells tested, 50 percent were excitable and displayed calcium-dependent action potentials when depolarized. When injected directly on the membrane of an excitable cell, thyrotropin-releasing hormone and 17 β-estradiol induced action potentials within 1 minute. The spiking activity was preceded by a progressive increase of the input resistance without any detectable change in the resting membrane polarization. The results reveal a rapid effect of both substances on the membrane of GH 3 /B6 cells. In the case of thyrotropin-releasing hormone, which has both a short-term effect on release of prolactin and a long-term effect on its synthesis, the induced electrical activity may be associated with the stimulation of prolactin production. The physiological implication of 17 β-estradiol-induced, calcium-dependent spiking activity remains to be elucidated.

Characterization of a Plasma Membrane Calcium Oscillator in Rat Pituitary Somatotrophs

“…High amplitude spontaneous [Ca 2ϩ ] i transients are not unique for somatotrophs, as immortalized pituitary cells also exhibit such changes (1)(2)(3)(4)(5)(6)(7)(8)(9)(10) influx in spontaneous and GHRH-controlled electrical activity in somatotrophs (19) and GC somatotroph lines (3).…”

“…The immortalized GH, 1 GS, AtT-20, and ␣T3 pituitary cells have been frequently used as cell models for the characterization of electrical activity and the associated Ca 2ϩ signaling in lactotrophs, somatotrophs, corticotrophs, and gonadotrophs, respectively (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). Simultaneous measurements of electrical activity and intracellular free Ca 2ϩ concentrations ([Ca 2ϩ ] i ) in GH 3 B 6 pituitary cells confirmed the dependence of [Ca 2ϩ ] i on action potential (AP) firing (1).…”

A Novel Taspine Derivative, HMQ1611, Inhibits Breast Cancer Cell Growth via Estrogen Receptor α and EGF Receptor Signaling Pathways

“…ERa is a member of the large superfamily of nuclear receptors acting as a ligand-activated transcription factor (4-7), which binds to 17b-estradiol (E2) and combines with specific estrogen response elements (ERE) in the promoters of target genes in the nucleus. In addition to this genomic mechanism of ERa, increasing experimental evidence has showed its nongenomic effect, which can be rapidly activated by estrogen (8)(9)(10)(11)(12). The membrane ERa can also transactivate insulin-like growth factor 1 receptor (IGF-1R) and EGF receptor (EGFR)/HER2, which leads to the activation of the downstream extracellular signal-regulated kinases (ERK) signaling cascade (13)(14)(15).…”

Thyrotropin releasing hormone stimulates metabolism of phosphatidyl inositol in GH3 cells

“…Ca z÷ influx into GH3 cells brought about by depolarization of the plasma membrane with high potassium, Abbreviations: PI, phosphatidylinositol; TRH, thyrotropin releasing hormone; PRL, prolactin; GH, growth hormone or by CaZ+-ionophores mimics a TRH response [4]. Electrophysiological experiments show an increase in calcium action potentials following TRH stimulation [5][6][7]. The mechanisms by which TRH modifies intracellular [Ca 2÷] are not known yet.…”