Calcium-activated potassium channels

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

“…Ca 2+ -activated K + currents: The model includes two Ca 2+ -activated K + currents mediated by SK and BK channels (Marty 1981;Marty and Neher 1985;Vergara et al 1998). Activation of the SK channels is voltage independent and highly sensitive to intracellular Ca 2+ (Hille 2001;Sah and Davies 2000); BK channel activation is both voltage-and Ca 2+ -dependent (Vergara et al 1998;Dopico et al 1999).…”

“…Activation of the SK channels is voltage independent and highly sensitive to intracellular Ca 2+ (Hille 2001;Sah and Davies 2000); BK channel activation is both voltage-and Ca 2+ -dependent (Vergara et al 1998;Dopico et al 1999). While activation of BK channels contributes to the falling phase of individual action potentials and the generation of the fast after hyperpolarizing potential (AHP) or hyperpolarizing after potential in many types of neurons (Lancaster and Adams 1986;Lancaster and Nicoll 1987;MacDermott and Weight 1982;Womack and Khodakhah 2002), including MNCs (Dopico et al 1999), SK channel activation is responsible for the generation of the AHP following a train of action potentials (Armstrong et al 1994;Bourque and Brown 1987;Greffrath et al 1998;Kirkpatrick and Bourque 1996;Lancaster and Adams 1986;Lancaster and Nicoll 1987;Sah and Bekkers 1996).…”

“…2(b)) were taken from data obtained in giant inside-out patches of Xenopus oocytes showing that all SK-channel subtypes exhibit similar Ca 2+ dose-response relationships, with a half-maximal activation of about 0.3 μM Ca 2+ and a Hill coefficient of about 4 (0.32±0.03 μM and 5.0±0.6 for SK3 channels) (see Appendix). BK channels are activated by an increase in intracellular [Ca 2+ ] and by depolarization (Vergara et al 1998), and the activation was described by a modified Boltzmann function:…”

Opposing effects of spinal nerve ligation on calcium-activated potassium currents in axotomized and adjacent mammalian primary afferent neurons

“…However, little is known about the role and contribution of these channels in the pathogenesis of neuropathic pain, although they may link reduced I Ca with neuronal hyper-excitability and other phenomena observed in neuropathic states. It is well known that K (Ca) channels regulate several functions pertinent to normal sensory as well as to neuropathic pain transduction, such as modulating AHP, controlling the repolarization and duration of the AP, suppressing membrane excitability, setting inter-spike interval, mediating spike-frequency adaptation and controlling neurotransmitter release [90]. Three major families of K (Ca) channels have been identified in neurons, each with distinct structure, and pharmacological and biophysical properties, including single-channel conductance in symmetrical K + solutions.…”

“…Three major families of K (Ca) channels have been identified in neurons, each with distinct structure, and pharmacological and biophysical properties, including single-channel conductance in symmetrical K + solutions. Largeconductance BK channels are voltage-gated and sensitive to iberiotoxin, whereas smallconductance SK channels are sensitive to apamin, and intermediate-conductance IK channels are sensitive to clotrimazole [22,77,78,90]. While BK channels require membrane depolarization for their activation, both SK and IK are voltage insensitive [17].…”