Neuron
ArticleAt least two mRNA species contribute to the properties of rat brain A-type potassium channel expressed in xenopus oocytes
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Cited by (88)
Conduits of life's spark: A perspective on ion channel research since the birth of neuron
2013, NeuronCitation Excerpt :In reflecting on the questions that motivated ion channel research 25 years ago, it is striking that the spirit, if not the details, of the studies exemplified in Neuron’s inaugural year mark many of the same questions that occupy the field today. These include: what is the physical nature of a channel (Auld et al., 1988; Ballivet et al., 1988; Deneris et al., 1988; Levitan et al., 1988; Lotan et al., 1988; Rudy et al., 1988; Timpe et al., 1988)? How do ions and pharmacological tools interact with channel pores (MacKinnon et al., 1988; Miller, 1988; Miller et al., 1988)?
Single cell analysis of voltage-gated potassium channels that determines neuronal types of rat hypothalamic paraventricular nucleus neurons
2012, NeuroscienceCitation Excerpt :In response to depolarizing from a hyperpolarizing membrane potential, PVN neurons displaying a delay in onset of the first action potential were classified as type I neurons, whereas PVN neurons not displaying a delay as type II neurons. 4-aminopyridine (4-AP), an A-type K+ channel blocker (Rudy et al., 1988), was obtained from Sigma-Aldrich (St. Louis, MO, USA) and was applied to the bath solution (ACSF) at the appropriate concentration. Single-cell RT-PCR was carried out as previously described with minor modifications (Glasgow et al., 1999; Di et al., 2003; Lee et al., 2008).
Dopamine D1-like receptor activation depolarizes medium spiny neurons of the mouse nucleus accumbens by inhibiting inwardly rectifying K<sup>+</sup> currents through a cAMP-dependent protein kinase A-independent mechanism
2010, NeuroscienceCitation Excerpt :Other candidates include the hyperpolarization-activated cyclic nucleotide-modulated channels (Robinson and Siegelbaum, 2003), but their expression within the NAc has been reported only in a minority of neurons that were identified not as MSNs but as cholinergic interneurons (Uchimura et al., 1990; Kawaguchi, 1993; Kawaguchi et al., 1995). Our biophysical and pharmacological analyses indicate that the mechanism underlying MSN depolarization is the inhibition of K+ conductances, which—given their Ba2+-sensitivity and inward rectification at hyperpolarized potentials—are probably of the Kir type (Rudy et al., 1988; Nichols and Lopatin, 1997; Hille, 2001). NAc neurons express several Kir channel subtypes, including the classic inward rectifier K+ channels (IRK1–3 or Kir 2.1–3) and G–protein–activated inward rectifiers (GIRK1 and 3, or Kir 3.1 and Kir 3.3) (Karschin et al., 1996; Mermelstein et al., 1998).
Multiple Kv channel-interacting proteins contain an N-terminal transmembrane domain that regulates Kv4 channel trafficking and gating
2008, Journal of Biological ChemistryCitation Excerpt :However, its presence does not strictly determine how channel properties are modified, resulting in a diversity of kinetic and voltage-dependent gating properties. Multiple KChIP Isoforms Have KISDs—The major focus for molecular studies on neuronal ISA has been on identifying auxiliary subunits that produce fast rapid activation and inactivation gating (25, 32, 33), making KChIP4a a curiosity among the ISA subunits. Here we show that KChIP4a is no lone oddball but rather is one member of a group of KChlPs that modify ISA channel expression and functional properties by providing an additional regulatory transmembrane domain that modifies the functional properties of the transmembrane pore gates.
A new mode of regulation of N-type inactivation in a Caenorhabditis elegans voltage-gated potassium channel
2007, Journal of Biological Chemistry