Reduced availability of voltage-gated sodium channels by depolarization or blockade by tetrodotoxin boosts burst firing and catecholamine release in mouse chromaffin cells

Knockout of the BK β2 subunit abolishes inactivation of BK currents in mouse adrenal chromaffin cells and results in slow-wave burst activity

(2014) Pedro L. Martinez-Espinosa et al.   JOURNAL OF GENERAL PHYSIOLOGY

Ligand-Gating by Ca2+ Is Rate Limiting for Physiological Operation of BKCa Channels

(2013) H. Berkefeld et al.   JOURNAL OF NEUROSCIENCE

Gap junction signalling is a stress-regulated component of adrenal neuroendocrine stimulus-secretion coupling in vivo

(2013) Michel G. Desarménien et al.   Nature Communications

Functional Chromaffin Cell Plasticity in Response to Stress: Focus on Nicotinic, Gap Junction, and Voltage-Gated Ca2+ Channels

(2012) Nathalie C. Guérineau et al.   JOURNAL OF MOLECULAR NEUROSCIENCE

CaV1.3-Driven SK Channel Activation Regulates Pacemaking and Spike Frequency Adaptation in Mouse Chromaffin Cells

(2012) D. H. F. Vandael et al.   JOURNAL OF NEUROSCIENCE

Pacemaker Rate and Depolarization Block in Nigral Dopamine Neurons: A Somatic Sodium Channel Balancing Act

(2012) K. R. Tucker et al.   JOURNAL OF NEUROSCIENCE

Are Cav1.3 pacemaker channels in chromaffin cells? Possible bias from resting cell conditions and DHP blockers usage

(2011) Satyajit Mahapatra et al.   Channels

Transcriptional up-regulation of cell surface NaV1.7 sodium channels by insulin-like growth factor-1 via inhibition of glycogen synthase kinase-3β in adrenal chromaffin cells: enhancement of 22Na+ influx, 45Ca2+ influx and catecholamine secretion

(2011) Toshihiko Yanagita et al.   NEUROPHARMACOLOGY

Loss of Cav1.3 Channels Reveals the Critical Role of L-Type and BK Channel Coupling in Pacemaking Mouse Adrenal Chromaffin Cells

(2010) A. Marcantoni et al.   JOURNAL OF NEUROSCIENCE

Cav1.3 and BK Channels for Timing and Regulating Cell Firing

(2010) David Henry Vandael et al.   MOLECULAR NEUROBIOLOGY

Control of transient, resurgent, and persistent current by open-channel block by Na channel  4 in cultured cerebellar granule neurons

(2010) J. S. Bant et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Sodium Entry during Action Potentials of Mammalian Neurons: Incomplete Inactivation and Reduced Metabolic Efficiency in Fast-Spiking Neurons

(2009) Brett C. Carter et al.   NEURON

PDE type-4 inhibition increases L-type Ca2+ currents, action potential firing, and quantal size of exocytosis in mouse chromaffin cells

(2008) A. Marcantoni et al.   PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY