z-logo
Premium
Estrogen regulation of ion channel expression mediating neuronal excitability in rat presympathetic PVN neurons
Author(s) -
Lee Seul Ki,
Ryu Pan Dong,
Lee So Yeong
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1091.49
Subject(s) - rostral ventrolateral medulla , endocrinology , medicine , nucleus , bursting , premovement neuronal activity , potassium channel , neuroscience , chemistry , patch clamp , estrogen receptor , medulla oblongata , neuronal firing , neuron , receptor , biology , electrophysiology , central nervous system , cancer , breast cancer
The hypothalamic paraventricular nucleus (PVN) is an important site in regulating the autonomic nervous system. Specifically, the PVN neurons projecting the rostral ventrolateral medulla (PVN‐RVLM) play a regulatory role in sympathetic outflow and their neuronal activities are influenced by A‐type potassium currents and T‐type calcium currents. It has been demonstrated that 17β‐estradiol (E 2 ) regulates neuronal excitability and estrogen receptor β is expressed in PVN‐RVLM neurons. We hypothesized that E 2 may regulate neuronal activity via the transcriptional regulation of ion channels expressed in PVN‐RVLM neurons. We investigated changes in firing rates and relative mRNA expressions of Kv4.2, Kv4.3, and Cav3.1 using whole cell patch clamp recording and single cell analysis. The results demonstrated that E 2 increased firing rates, and altered mRNA expressions of Kv4.2 and Cav3.1 in PVN‐RVLM neurons. These results suggest that E 2 increased the neuronal excitability by mediating Kv4.2 and Cav3.1 expressions in PVN‐RVLM neurons. This study received support from the National Research Foundation of Korea (2010‐0017216).

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here