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Volume 91, Issue 1

1 January 1988

Journal of General Physiology Cover Image for Volume 91, Issue 1

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ISSN 0022-1295

EISSN 1540-7748

In this Issue

Article

Article

Two ATP-activated conductances in bullfrog atrial cells.

D D Friel,B P Bean

View Articletitled, Two ATP-activated conductances in bullfrog atrial cells.

Receptor current fluctuation analysis in the labellar sugar receptor of the fleshfly.

H Kijima,K Nagata,A Nishiyama,H Morita

View Articletitled, Receptor current fluctuation analysis in the labellar sugar receptor of the fleshfly.

Membrane currents in retinal bipolar cells of the axolotl.

M Tessier-Lavigne,D Attwell,P Mobbs,M Wilson

View Articletitled, Membrane currents in retinal bipolar cells of the axolotl.

Voltage-dependent K+ currents and underlying single K+ channels in pheochromocytoma cells.

T Hoshi,R W Aldrich

View Articletitled, Voltage-dependent K+ currents and underlying single K+ channels in pheochromocytoma cells.

Gating kinetics of four classes of voltage-dependent K+ channels in pheochromocytoma cells.

T Hoshi,R W Aldrich

View Articletitled, Gating kinetics of four classes of voltage-dependent K+ channels in pheochromocytoma cells.

Spontaneous Ca2+ release from the sarcoplasmic reticulum limits Ca2+-dependent twitch potentiation in individual cardiac myocytes. A mechanism for maximum inotropy in the myocardium.

M C Capogrossi,M D Stern,H A Spurgeon,E G Lakatta

View Articletitled, Spontaneous Ca2+ release from the sarcoplasmic reticulum limits Ca2+-dependent twitch potentiation in individual cardiac myocytes. A mechanism for maximum inotropy in the myocardium.

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TREK-1 channels regulate pressure sensitivity and calcium signaling in trabecular meshwork cells

The physical basis of osmosis

Voltage-Gated Na Channels

Drugs exhibit diverse binding modes and access routes in the Na_v1.5 cardiac sodium channel pore

Probenecid affects muscle Ca²⁺ homeostasis and contraction independently from pannexin channel block

Mechanotransduction by Membrane Proteins

Mechanosensitive channel MscS is critical for termination of the bacterial hypoosmotic permeability response

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