Kir Channels In Multi-Cellular Organisms

Potassium in the human body is largely located in the cells as the major cation of the intracellular fluid. There is also a small amount of potassium in the

The voltage gated potassium-complex are made of single ion pore with subunits. Located in the postsynaptic fold. The voltage gated potassium complex has a significant amount of roles such

1. ECF potassium levels affect resting membrane potential. Hyperkalemia (excessive levels of potassium in the blood) and hypokalemia (abnormally low blood potassium levels) both affect the function of nerves and muscles.

Increasing the extracellular potassium reduces the concentration gradient, and less potassium diffuses out of the neuron and into the cell.

This experiment seeks to analyze how the resting membrane potential of Orconectes rusticus muscle cells changes in response to increasing [K+]o solution concentrations. By recording the intracellular voltage of the DEM, DEL1, and DEL2 crayfish muscle cells at six concentrations of [K+]o solution, we determined whether the observed resting membrane potentials (Vrest) were significantly different from the predicted Nernst equilibrium potential values. We hypothesized that the Vrest of the crayfish muscles at each concentration would not significantly differ from the Nernst potential, which solely considers the permeability of potassium ions to the cell membrane. However, our findings suggested differently, and results indicated that the Nernst equation did not accurately predict the obtained values of the resting membrane potential. The differences in muscle cell Vrest reveal instead that the membrane is differentially permeable to other ions.

Explain why increasing extracellular K+ reduces the net diffusion of K+ out of the neuron through the K+ leak channels.

-If the potassium transport pump was blocked the leakage channels would still be open allowing Na+ to

Hyperkalemic Periodic Paralysis Disease (HYPP) is a muscular disorder found prominently in horses that occurs due to an inherited genetic mutation [1]. Specifically, a point mutation in the sodium channel gene, found in the muscle of affected horses, is passed on to offspring [1]. Sodium channels found in the muscle cell membrane primarily control muscle fiber contraction [1]. According to research summarized by UC Davis, when this defective sodium channel gene is present, the channels “leak” due to fluctuation of blood potassium levels, causing the muscle to depolarize and to contract involuntarily [4]. These fluctuating potassium levels may result from a period of fasting, followed by intake of high potassium feed, such as alfalfa [1]. Ultimately, the depolarization causes the muscles to lose their effectiveness, and myopathy eventually develops [4]. All horses positive for the HYPP gene mutation are affected for their entire lives [2].

They are classified according to the trigger that opens the channel for such ions, either a voltage change or a binding of a substance to the ligand-gated sodium channels. Sodium channels consist of a large α subunit that associates with other proteins, such as β subunits. An α subunit forms the core of the channel and is functional on its own. When the α subunit protein is expressed by a cell, it is able to form channels that conduct Na+ in a voltage-gated way, even if β subunits or other known modulating proteins are not expressed. When accessory proteins assemble with α subunits, the resulting complex can display altered voltage dependence and cellular localization. Binding of natural brevetoxins to voltage-sensitive sodium channels (VSSC) results in a cadre of four distinct effects: a shifting of the activation potential to more negative values; prolonged channel open times; inhibition of inactivation; and induction of subconductance states. Individual brevetoxins exhibit differential sodium channel binding affinities and potencies. Differences in affinity of the natural toxins have been attributed to variations in lipophilicity, topographic features relative to the binding site, and differential toxicities based on affinity governed by specific molecular or structural differences of each toxin. Regardless of affinity, all toxins affect

Increasing extracellular K+ causes the membrane potential to change to a less negative value because the K+ ions diffuse out across the membrane. My results went well compared to my prediction because I predicted that the resting membrane potential would become less negative.

The findings of this experiment reinforced the hypothesis that the resting membrane potential is most influenced by the ion potassium. We were able to deduce this through the collection of a multitude of intracellular and extracellular recordings, such as the one shown below in Figure 1. This shows how this experiment was able to record every single resting membrane potential in all three different muscle groups under all six solutions.

SCN5a is part of a family of 10 genes that encode different types of sodium channels, i.e. brain-type (NaV1.1, NaV1.2, NaV1.3, NaV1.6), neuronal channels (NaV1.7, NaV1.8 and NaV1.9), skeletal muscle channels (NaV1.4) and the cardiac sodium channel NaV1.5. problems (Park & Fishman, 2011).” The SCN5A gene encodes for the alpha subunit of the cardiac sodium channel (Yan & Antzelevitch 1999). This gene is an autosomal dominant gene which means a person only has to carry one copy of the mutated gene to experience common one of the common arrhythmia, asymptomatic or ultimately a cardiac

CNGA3 associated achromatopsia makes up 30% of all known cases of achromatopsia and is known as achromatopsia 2. Hereditary ion channelopathies of the central nervous system and visual systems are so damaging because they start to show up when the patient is an infant or early in their childhood. Because these types of disorders are so rare there is very limited access to affected tissues which makes answering basic questions about how the disease works and develop extremely difficult. The development of therapeutic approaches to treating achromatopsia patients such as gene replacement therapy or understanding parts of the complex function of the disease strongly rely on using animal

Fun facts: Based on transferring sodium and potassium ions cross the plasma membrane, the aquaporins channels(also called water channels) will now become active and responsible for absorbing water and this is the reason why a host of sports drinks contain sodium and potassium ions that will help with the body water absorption.

Despite the various roles for STIM and Orai dependent channels, it is primarily the store-operated channels for which there is information regarding roles in physiological processes. For example, to the author’s knowledge, no publications have appeared utilizing animal models to investigate the importance of ARC channels or SOC channels at the organ system or organism level. Animal models with TRPC channel deletions have revealed numerous physiological functions subtended by these channels, but without experimentally demonstrating that these involve the store-operated activation mode.