International Geomagnetic Reference Field: the thirteenth generation

In December 2019, the International Association of Geomagnetism and Aeronomy (IAGA) Division V Working Group (V-MOD) adopted the thirteenth generation of the International Geomagnetic Reference Field (IGRF). This IGRF updates the previous generation with a definitive main field model for epoch 2015.0, a main field model for epoch 2020.0, and a predictive linear secular variation for 2020.0 to 2025.0. This letter provides the equations defining the IGRF, the spherical harmonic coefficients for this thirteenth generation model, maps of magnetic declination, inclination and total field intensity for the epoch 2020.0, and maps of their predicted rate of change for the 2020.0 to 2025.0 time period

β-Arrestin Regulates Estradiol Membrane-Initiated Signaling in Hypothalamic Neurons

Estradiol (E2) action in the nervous system is the result of both direct nuclear and membrane-initiated signaling (EMS). E2 regulates membrane estrogen receptor-α (ERα) levels through opposing mechanisms of EMS-mediated trafficking and internalization. While ß-arrestin-mediated mERα internalization has been described in the cortex, a role of ß-arrestin in EMS, which underlies multiple physiological processes, remains undefined. In the arcuate nucleus of the hypothalamus (ARH), membrane-initiated E2 signaling modulates lordosis behavior, a measure of female sexually receptivity. To better understand EMS and regulation of ERα membrane levels, we examined the role of ß-arrestin, a molecule associated with internalization following agonist stimulation. In the present study, we used an immortalized neuronal cell line derived from embryonic hypothalamic neurons, the N-38 line, to examine whether ß-arrestins mediate internalization of mERα. β-arrestin-1 (Arrb1) was found in the ARH and in N-38 neurons. In vitro, E2 increased trafficking and internalization of full-length ERα and ERαΔ4, an alternatively spliced isoform of ERα, which predominates in the membrane. Treatment with E2 also increased phosphorylation of extracellular-signal regulated kinases 1/2 (ERK1/2) in N-38 neurons. Arrb1 siRNA knockdown prevented E2-induced ERαΔ4 internalization and ERK1/2 phosphorylation. In vivo, microinfusions of Arrb1 antisense oligodeoxynucleotides (ODN) into female rat ARH knocked down Arrb1 and prevented estradiol benzoate-induced lordosis behavior compared with nonsense scrambled ODN (lordosis quotient: 3 ± 2.1 vs. 85.0 ± 6.0; p < 0.0001). These results indicate a role for Arrb1 in both EMS and internalization of mERα, which are required for the E2-induction of female sexual receptivity