Single-channel properties of BK-type calcium-activated potassium channels at a cholinergic presynaptic nerve terminal

The presynaptic nerve terminal is of key importance in the communication in the nervous system. Its primary role is to release transmitter quanta on the arrival of an appropriate stimulus. The structural basis of these transmitter quanta are the synaptic vesicles that fuse with the surface membrane of the nerve terminal, to release their content of neurotransmitter molecules and other vesicular components. We subdivide the control of quantal release into two major classes: the processes that take place before the fusion of the synaptic vesicle with the surface membrane (the pre–fusion control) and the processes that occur after the fusion of the vesicle (the post–fusion control). The pre–fusion control is the main determinant of transmitter release. It is achieved by a wide variety of cellular components, among them the ion channels. There are reports of several hundred different ion channel molecules at the surface membrane of the nerve terminal, that for convenience can be grouped into eight major categories. They are the voltage–dependent calcium channels, the potassium channels, the calcium–gated potassium channels, the sodium channels, the chloride channels, the non–selective channels, the ligand gated channels and the stretch–activated channels. There are several categories of intracellular channels in the mitochondria, endoplasmic reticulum and the synaptic vesicles. We speculate that the vesicle channels may be of an importance in the post–fusion control of transmitter release.

Download Full-text

Single-channel biophysical and pharmacological characterizations of native human large-conductance calcium-activated potassium channels in freshly isolated detrusor smooth muscle cells

Pflügers Archiv - European Journal of Physiology ◽

10.1007/s00424-012-1214-8 ◽

2013 ◽

Vol 465 (7) ◽

pp. 965-975 ◽

Cited By ~ 13

Author(s):

John Malysz ◽

Eric S. Rovner ◽

Georgi V. Petkov

Keyword(s):

Smooth Muscle ◽

Potassium Channels ◽

Smooth Muscle Cells ◽

Single Channel ◽

Muscle Cells ◽

Detrusor Smooth Muscle ◽

Calcium Activated Potassium Channels ◽

Detrusor Smooth Muscle Cells

Download Full-text

Oscillations in the activity of a potassium channel at the presynaptic nerve terminal

Journal of Neurophysiology ◽

10.1152/jn.1995.73.6.2448 ◽

1995 ◽

Vol 73 (6) ◽

pp. 2448-2458 ◽

Cited By ~ 6

Author(s):

R. Rahamimoff ◽

J. Edry-Schiller ◽

M. Rubin-Fraenkel ◽

A. Butkevich ◽

S. Ginsburg

Keyword(s):

Potassium Channels ◽

Single Channel ◽

Electric Organ ◽

Oscillatory Behavior ◽

Experimental Conditions ◽

Periodic Oscillations ◽

Presynaptic Nerve Terminal ◽

Random Behavior ◽

Torpedo Electric Organ ◽

Membrane Oscillations

1. Periodic oscillations were detected in the activity of single macromolecules: potassium channels. 2. When potassium channels are repeatedly activated in isolated patches from fused synaptosomes of Torpedo electric organ, their behavior exhibits a departure from random activation. 3. The departure from random behavior is demonstrated by the runs test and by the lack of fit to Poisson distribution. 4. Under appropriate experimental conditions, the channels display periodic oscillations with a periodicity of approximately 20 s when activated at a rate of 1.25 Hz. 5. The oscillations do not arise from sampling, recording, or computational artifacts. 6. It is conceivable that single-channel oscillations play a role in the generation of membrane oscillations and thus may contribute to the oscillatory behavior of the nervous system.

Download Full-text

Calcium-activated potassium channels and nitric oxide coregulate estrogen-induced vasodilation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.1.h319 ◽

2000 ◽

Vol 279 (1) ◽

pp. H319-H328 ◽

Cited By ~ 71

Author(s):

Charles R. Rosenfeld ◽

Richard E. White ◽

Tim Roy ◽

Blair E. Cox

Keyword(s):

Nitric Oxide ◽

Heart Rate ◽

Potassium Channels ◽

Uterine Artery ◽

Single Channel ◽

Open Probability ◽

Calcium Dependent ◽

Calcium Activated Potassium Channels ◽

Artery Flow ◽

Oxide Synthase

Nitric oxide synthase (NOS) contributes to estradiol-17β (E2β)-induced uterine vasodilation, but additional mechanisms are involved, and the cellular pathways remain unclear. We determined if 1) uterine artery myocytes express potassium channels, 2) E2β activates these channels, and 3) channel blockade plus NOS inhibition alters E2β-induced uterine vasodilation. Studies of cell-attached patches identified a 107 ± 7 pS calcium-dependent potassium channel (BKCa) in uterine artery myocytes that rapidly increased single-channel open probability 70-fold ( P < 0.05) after exposure to 100 nM E2β through an apparent cGMP-dependent mechanism. In ovariectomized nonpregnant ewes ( n = 11) with uterine artery flow probes and catheters, local BKCa blockade with tetraethylammonium (TEA; 0.05–0.6 mM) dose dependently inhibited E2β-induced uterine vasodilation ( n = 37, R = 0.77, P < 0.0001), with maximum inhibition averaging 67 ± 11%. Mean arterial pressure (MAP) and E2β-induced increases ( P ≤ 0.001) in heart rate (13%) and contralateral uterine blood flow (UBF, ∼5-fold) were unaffected. Local NOS inhibition plus BKCa blockade, using submaximal doses of nitro-l-arginine methyl ester (5 mg/ml) and TEA (0.3 mM), did not alter basal UBF but completely inhibited ipsilateral E2β-induced uterine vasodilation without affecting MAP and E2β-induced increases in contralateral UBF and heart rate. Acute E2β-mediated uterine vasodilation involves rapid activation of uterine artery BKCa and NOS, and the pathway for their interaction appears to include activation of guanylyl cyclase.

Download Full-text