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potassium channel, subfamily T, member 2
KNa channels were first identified in guinea pig cardiomyocytes (Kameyama et al., 1984 ). Subsequently, similar channels were reported in a variety of neurons (Bader et al., 1985 ; Dryer et al., 1989 ; Schwindt et al., 1989 ; Dryer, 1991 ; Egan et al., 1992a ; Haimann et al., 1992 ; Dale, 1993 [13; Safronov and Vogel, 1996 ; Bischoff et al., 1998 ). Like Ca2+ -activated BK and SK channels, the properties of KNa channels appear to be diverse. The reported unitary conductances of these channels range from 105 to 200 pS, and half-maximal activation by Na+ occurs between 7 and 80 mM, depending on cell type and recording conditions (Dryer, 1994 ).
KCNT2 (also known as SLICK; KCa4.2; SLO2.1; MGC119610; MGC119611; MGC119612; MGC119613; RP11-58O13.1) encodes Slo2b, a potassium channel, subfamily T, member 2.
Kcnt2 : potassium channel, subfamily T, member 2
The activity of Slick channels is substantially more sensitive than Slack to changes in intracellular Cl-, and Slick open probability is significant even in the absence of Na+. Moreover, Slick contains a regulatory nucleotidebinding site that is responsible for ATP-dependent inhibition of channel activity. (Bhattacharjee )
Slick (Slo2.1) is selectively expressed in the nervous system and heart. (Bhattacharjee )
The physiological roles of KNa channels (such as Slo2b) appear to be distinct in different cell types. For example, in quail trigeminal ganglion neurons and in dorsal root ganglion neurons, it has been suggested that KNa channels regulate the resting membrane potential (Haimann et al., 1992 ; Bischoff et al., 1998 ). In other neurons, KNa channels have been implicated in an apamin-insensitive, Na+-dependent slow afterhyperpolarization (AHP) that follows a burst of action potentials (Dryer, 1994 ). In ferret perigeniculate neurons, such a Na+-dependent slow AHP is an important component of spindle wave activity (Kim and McCormick, 1998 ). It has also been proposed that KNa channels may be activated by a single action potential and may therefore play a role in determining the duration of action potentials (Bertrand et al., 1989 ), although is unclear whether the amount of Na+ influx through a TTX-sensitive Na+ channel during a single action potential is normally sufficient to activate KNa channels (Dryer, 1994 , 1991 ). Activation may depend on the relative rates of influx, diffusion, and extrusion of Na+, the proximity of KNa channels to the source of Na+, and the particular geometry of the space occupied by KNa channels in a given cell type (Dryer, 1994 , 1991 ).
The properties of the Slick channel indicate that its activation by intense neuronal activity or by hypoxia may hyperpolarize specific neurons in the brain and the heart, where the channel is expressed, thereby limiting excitability and energy consumption to maintain cell viability. (Bhattacharjee )
With similar single-channel conductance to Slack, Slick also rectifies outwardly and is activated by intracellular Na+. In marked contrast to Slack, however, Slick activation occurs very rapidly with step changes in voltage, whereas Slack activation increases with time after a step depolarization. (Bhattacharjee )