In proestrus, the changing gonadal hormone milieu alters the physiological properties of GnRH neurons and contributes to the development of the GnRH surge. We hypothesized that proestrus also influences the expression of different ion channel genes in mouse GnRH neurons. Therefore, we performed gene expression profiling of GnRH neurons collected from intact, proestrous and metestrous GnRH-GFP transgenic mice, respectively. Proestrus changed the expression of 37 ion channel and 8 calcium homeostasis-regulating genes. Voltage-gated sodium channels responded with upregulation of three alpha subunits (, , and ). Within the voltage-gated potassium channel class, , , , and were upregulated, while others (, , , and ) underwent downregulation. Proestrus also had impact on inwardly rectifying potassium channel subunits manifested in enhanced expression of and genes, whereas , , and subunit genes were downregulated. The two-pore domain potassium channels also showed differential expression with upregulation of and reduced expression of three subunit genes (, , and ). Changes in expression of chloride channels involved both the voltage-gated ( and ) and the intracellular () subtypes. Regarding the pore-forming alpha-1 subunits of voltage-gated calcium channels, two ( and ) were upregulated, while showed downregulation. The ancillary subunits were also differentially regulated (, , , , , , , and ). In addition, ryanodine receptor 1 () gene was downregulated, while a transient receptor potential cation channel () gene showed enhanced expression. Genes encoding proteins regulating the intracellular calcium homeostasis were also influenced (, , , , , , and ). The differential expression of genes coding for ion channel proteins in GnRH neurons at late proestrus indicates that the altering hormone milieu contributes to remodeling of different kinds of ion channels of GnRH neurons, which might be a prerequisite of enhanced cellular activity of GnRH neurons and the subsequent surge release of the neurohormone.
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| http://dx.doi.org/10.3389/fnmol.2019.00137 | DOI Listing |
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