Toggle Main Menu Toggle Search

Open Access padlockePrints

A constitutively active nonselective cation conductance underlies resting Ca2+ influx and secretion in bovine adrenal chromaffin cells

Lookup NU author(s): Dr Tim Cheek


Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


We have combined fluorimetric measurements of the intracellular free Ca2+ concentration ([Ca2+]i) with the patch clamp technique, to investigate resting Ca2+ entry in bovine adrenal chromaffin cells. Perfusion with nominally Ca2+-free medium resulted in a rapid, reversible decrease in [Ca2+]i, indicating a resting Ca2+ permeability across the plasma membrane. Simultaneous whole-cell voltage-clamp showed a resting inward current that increased when extracellular Ca2+ (Ca2+o) was lowered. This current had a reversal potential of around 0 mV and was carried by monovalent or divalent cations. In Na+-free extracellular medium there was a reduction in current amplitude upon removal of Ca2+o, indicating the current can carry Ca2+. The current was constitutively active and not enhanced by agents that promote Ca2+-store depletion such as thapsigargin. Extracellular La3+ abolished the resting current, reduced resting [Ca2+]i and inhibited basal secretion. Abolishment of resting Ca2+ influx depleted the inositol 1,4,5-trisphosphate-sensitive Ca2+ store without affecting the caffeine-sensitive Ca2+ store. The results indicate the presence of a constitutively active nonselective cation conductance, permeable to both monovalent and divalent cations, that can regulate [Ca2+]i, the repletion state of the intracellular Ca2+ store and the secretory response in resting cells. © 2006 Elsevier Ltd. All rights reserved.

Publication metadata

Author(s): Cheek TR, Thorn P

Publication type: Article

Publication status: Published

Journal: Cell Calcium

Year: 2006

Volume: 40

Issue: 3

Pages: 309-318

ISSN (print): 0143-4160

ISSN (electronic): 1532-1991

Publisher: Elsevier


DOI: 10.1016/j.ceca.2006.04.002

PubMed id: 16806464


Altmetrics provided by Altmetric


Funder referenceFunder name
G0000190Medical Research Council
G0400669Medical Research Council