Erg currents support electrical bursting in murine anterior pituitary corticotrophs.
Overview
- Institute for Neuroscience and Cardiovascular Research Edinburgh Medical School University of Edinburgh Edinburgh UK
- Department of Mathematics and Programs in Molecular Biophysics and Neuroscience Florida State University Tallahasee Florida USA
Abstract
Abstract: The regulation of electrical excitability of anterior pituitary corticotrophs is critical for an appropriate response of the hypothalamic‐pituitary‐a
We reveal that Kcnh2 is the major Eag‐channel family member mRNA expressed in male and female murine corticotrophs. Patch clamp electrophysiological analysis revealed corticotrophs exhibit robust Erg‐like currents that are inhibited by the selective Erg‐inhibitor E4031 but are not regulated by the major hypothalamic secretagogues, corticotrophin releasing hormone (CRH) or arginine vasopressin (AVP), that increase corticotroph excitability. Pharmacological inhibition of Erg currents had no effect on spontaneous electrical excitability in corticotrophs. Rather, paradoxically, Erg currents were important for supporting CRH‐induced bursting, similar to the role of large‐conductance calcium‐ and voltage‐activated potassium (BK) channels, providing a level of redundancy to control bursting. Indeed mathematical modelling revealed that in the absence of BK channels CRH‐induced bursting can be supported in thepresence of Erg current.
We thus reveal a novel role for Erg‐like channels in controlling CRH‐induced bursting in murine anterior pituitary corticotrophs that is likely to be an important determinant of HPA axis regulation in health and disease.
Key points: Voltage‐gated ether‐à‐go‐go‐related (Erg) potassium channels are key determinants of cellular excitability; however their functional role in native anterior pituitary cells remains poorly understood. Male and female murine corticotrophs predominantly express Kcnh2 (Erg1) mRNA, and electrophysiological recordings reveal functional Erg‐like potassium currents sensitive to the Erg inhibitor E4031. Erg currents do not control the basal electrical excitability of corticotrophs. We reveal a novel role for Erg currents in supporting electrical bursting in corticotrophs induced by the hypothalamic secretagogue, corticotrophin releasing hormone (CRH). Bursting in corticotrophs can be supported by both Erg and BK channels revealing a level of redundancy to the CRH response that will be critical for understanding the role of Erg channels in control of the stress axis in health and disease.
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Data
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Data availability statement
Data supporting the results presented in this article are included in the figures. Computer codes for model are available at www.math.fsu.edu/
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Version 2, 28 September 2026
- Publisher: n/a → Wiley
Version 1, 28 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 6 authors, 7 keywords, 10 MeSH terms, 2 funders, 43 references.
Cite
This paper
Nair, S. V., Romanò, N., Duncan, P. J., Tissier, P. L., Bertram, R., & Shipston, M. J. (2026). Erg currents support electrical bursting in murine anterior pituitary corticotrophs. The Journal of physiology, 604(12), 4834-4850. https://
BibTeX
@article{nair2026erg,
author = {Nair, Sooraj V. and Romanò, Nicola and Duncan, Peter J. and Tissier, Paul Le and Bertram, Richard and Shipston, Michael J.},
title = {{Erg currents support electrical bursting in murine anterior pituitary corticotrophs}},
journal = {The Journal of physiology},
year = {2026},
month = may,
volume = {604},
number = {12},
pages = {4834--4850},
publisher = {Wiley},
issn = {0022-3751},
doi = {10.1113/
url = {https://
pmid = {42113960},
pmcid = {PMC13267669}
}
RIS
TY - JOUR
AU - Nair, Sooraj V.
AU - Romanò, Nicola
AU - Duncan, Peter J.
AU - Tissier, Paul Le
AU - Bertram, Richard
AU - Shipston, Michael J.
TI - Erg currents support electrical bursting in murine anterior pituitary corticotrophs
T2 - The Journal of physiology
J2 - J Physiol
PY - 2026
DA - 2026/
VL - 604
IS - 12
SP - 4834
EP - 4850
SN - 0022-3751
PB - Wiley
DO - 10.1113/
UR - https://
LA - en
ER -
CSL-JSON
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