K+ channels regulation

SKca and M channels are not the only K+ channels regulated by transmitters. As noted above, transmitters can also close, or open, other K+ channels that do not directly regulate excitability but instead determine the resting potential of the neuron, and hence depolarise or hyperpolarise the neuron. 

Petkov GV, Bonev AD, Heppner TJ, Brenner R, Aldrich RW, Nelson MT 2001 / l-subunit of the Ca2+-activated K+ channel regulates contractile activity of mouse urinary bladder smooth muscle. J Physiol 537 443-452... 

Fernandez-Veledo, S., Casado, V., Norman, R.I.. Casado, F.J., lluis, C., Franco, R., and Pastor-Ariglada, M. (2004) ATP-sensitive K channels regulate the concentrative adenosine transporter CNT2 following activation hy A] adenosine receptors. Molecular and Cellular Biology, 24 (7), 2710-2719. 

Abbott GW (2016) KCNEl and KCNE3 the yin and yang of voltage-gated K(+) channel regulation. Gene 576 1-13... 

ATP-sensitive K+ channel ATP-regulated K+ channel Kaxp channel SURx/Kir6.x channel... 

Bryan J, Munoz A, Zhang X et al (2007) ABCC8 and ABCC9 ABC transporters that regulate K+ channels. Pfliigers Arch 453 703-718... 

Dopamine Di Dz, D4 D3 Gs Go, Gi G, Stimulates adenylyl cyclase raising cAMP Inhibits adenylyl cyclase, Ca +/K+ channels Phospholipase-C to IPsto [Ca +]i regulation... 

Glutamate-metabotropic mGluRl, 3, 5 mGluR2, 4, 6, 7 G, Go, Gi Phospholipase-C to IP3 to [Ca +]i regulation Inhibits adenylyl cyclase, Ca /K channels... 

Inclusion of Ca in the efflux media enhanced 86Rb efflux in 100 mM [K]0 but not 5 mM [K]0 (data not shown). This Ca-dependent 86Rb efflux (component "C") appears to be a manifestation of TEA-sensi-tive, Ca-regulated K channels (Bartschat and Blaustein 1985a Bartschat and Blaustein 1985b). 

The aforementioned results are consistent with the view that the rat brain PCP/"sigma opiate" high-affinity receptor is associated with the voltage-regulated, non inactivating K channels in the pre-synaptic terminals. Thus, we reasoned that the elucidation of the molecular composition of this PCP "receptor" might provide direct information about the subunit composition of these K channels. 

The behavioral effects of PCP have been associated with excessive release of a wide variety of neurotransmitters in particular, a massive dopamine release may underlie some of the most prominent symptoms of PCP intoxication (Rappolt et al. 1980). Our results readily explain the genesis of such an effect, because activation of presynaptic K channels is one of the primary factors that influences Ca entry into nerve terminals and Ca-dependent transmitter release by limiting action-potential duration and regulating excitabi1ity. 

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