Rapid Signaling of Estrogen in Hypothalamic Neurons Involves a Novel G-Protein-Coupled Estrogen Receptor that Activates Protein Kinase C

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Figure 1.
Figure 1.

17β-Estradiol and SERMs attenuate the GABAB response in hypothalamic neurons. A, Schematic showing the protocol for drug administration in the whole-cell patch voltage-clamp experiments (Vhold, -60 mV). After seals were formed and the whole-cell configuration was obtained, slices were perfused with TTX (1 μm) for 5 min. The first GABAB receptor-mediated response was generated by perfusing baclofen (at EC50 concentration of 5 μm) until a steady-state outward current was obtained (R1). After drug washout, the current returned to its predrug resting level. The cells were then treated with E2 and/or other drugs for 15 min, baclofen (5 μm) was perfused again, and R2 was measured. The effects of estrogen or other drugs on the baclofen response are expressed as a percentage of R2 over R1. B, An example of a biocytin-filled neuron after whole-cell patch-clamp recording for 13 min, illustrating the extent of the biocytin labeling. The slice was fixed immediately after the recording. C, The prebaclofen and postbaclofen (5 μm) I/V relationships from a dopamine neuron. The reversal potential for the outward current was close to the predicted equilibrium potential for potassium. D, The prebaclofen and postbaclofen I/V relationships after E2 treatment in another cell, illustrating the same reversal potential for the baclofen response. I/Vs were done before and after each drug treatment, and none of the drug treatments had any effect on the reversal potential for the baclofen response.

  1. The Journal of Neuroscience vol. 23 no. 29 9529-9540
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