** Inward-rectifier potassium channels: These channels allow potassium to flow into the cell in an inwardly rectifying manner, i. e., potassium flows effectively into, but not out of, the cell.

** Calcium-activated potassium channels: This family of channels is, for the most part, activated by intracellular Ca < sup > 2 +</ sup > and contains 8 members.

** Two-pore-domain potassium channels: This family of 15 members form what is known as leak channels, and they follow Goldman-Hodgkin-Katz ( open ) rectification.

** Voltage-gated potassium channels e. g., Kvs, Kirs etc.

** Calcium-activated potassium channels e. g., BKCa or MaxiK, SK, etc.

** Two-pore-domain potassium channels: This family of 15 members form what is known as leak channels, and they follow Goldman-Hodgkin-Katz ( open ) rectification.

** Phosphorylation of Na < sup >+</ sup >/ K < sup >+</ sup >- ATPase during the transport of sodium ( Na < sup >+</ sup >) and potassium ( K < sup >+</ sup >) ions across the cell membrane in osmoregulation to maintain homeostasis of the body's water content.

** niter, the mineral form of potassium nitrate

** the scala media ( containing endolymph ), or cochlear duct, a region of high potassium ion concentration that the cilia of the hair cells project into

** Cream of tartar ( potassium bitartrate )

** Tartar emetic ( antimony potassium tartrate )

** Severe potassium deficiency

** 10 – 36 mmol / L potassium ( higher than plasma )

** caution must be taken to prevent potassium or magnesium depletion

** Hydrogen potassium ATPase

** Hyperkalemia – A small rise of 0. 5 mmol / l occurs normally, this is of little consequence unless potassium is already raised such as in renal failure

** Hyperkalemia – Exaggerated potassium release in burn patients ( occurs from 24 hours after injury, lasting for up to 2 years ), neuromuscular disease and paralyzed ( quadraplegic, paraplegic ) patients.

** potassium > 6 meq / L or 25 % increase

** Creatinine, urea / blood urea nitrogen, sodium, potassium, chloride, bicarbonate, calcium, magnesium, phosphate

** 8 barrels of potassium chlorate each containing 1cwt, 1 large quantity of powdered charcoal, and 40 sticks of gelignite were uncovered.

** Arrests were made, with 1 London man charged with possession of 2 tons of potassium chlorate and 1 ton of iron oxide between 1 October and 5 November 1938.

** 2 tons of potassium chlorate & oxide of iron

** Cation channels of sperm: This small family of channels, normally referred to as Catsper channels, is related to the two-pore channels and distantly related to TRP channels.

** Cyclic nucleotide-gated channels: This family of channels is characterized by activation due to the binding of intracellular cAMP or cGMP, with specificity varying by member.

** Hyperpolarization-activated cyclic nucleotide-gated channels

** voltage-gated sodium channels NaVs

** epithelial sodium channels ( ENaC )

** Voltage-gated proton channels

** Most Transient receptor potential channels

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Sodium, calcium, and potassium channels are all implicated in contributing to input modulation.

2-pore-domain potassium channels, with the subfamilies TREK and TASK, have recently emerged as a potential target.

* G < sub > βγ </ sub > sometimes also have active functions, e. g., coupling to and activating G protein-coupled inwardly-rectifying potassium channels.

* Voltage-gated potassium channels ( K < sub > V </ sub >): This family contains almost 40 members, which are further divided into 12 subfamilies.

* Some potassium channels

* Dendrotoxin is produced by mamba snakes, and blocks potassium channels.

* Iberiotoxin is produced by the Buthus tamulus ( Eastern Indian scorpion ) and blocks potassium channels.

* Heteropodatoxin is produced by Heteropoda venatoria ( brown huntsman spider or laya ) and blocks potassium channels.

* Long QT syndrome is a ventricular arrhythmia syndrome caused by mutations in one or more of presently ten different genes, most of which are potassium channels and all of which affect cardiac repolarization.

All neurons are electrically excitable, maintaining voltage gradients across their membranes by means of metabolically driven ion pumps, which combine with ion channels embedded in the membrane to generate intracellular-versus-extracellular concentration differences of ions such as sodium, potassium, chloride, and calcium.