Results 161 to 170 of about 5,036 (195)
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Effects of Orexin (Hypocretin) on GIRK Channels

Journal of Neurophysiology, 2003
Orexins (hypocretins) are recently discovered excitatory transmitters implicated in arousal and sleep. Yet, their ionic and signal transduction mechanisms have not been fully clarified. Here we show that orexins suppress G-protein–coupled inward rectifier (GIRK) channel activity, and this suppression is likely to lead to neuronal excitation.
Q V, Hoang   +4 more
openaire   +2 more sources

Heartfelt crosstalk: desensitization of the GIRK current

Nature Cell Biology, 2000
Acetylcholine calms the heartbeat by activating Gi-coupled receptors and G-protein-activated inwardly rectifying potassium (GIRK) channels. It also dampens the GIRK current by reducing PIP2 through Gq-coupled receptors. These two types of receptors seem to be engaged in an intriguingly specific form of crosstalk, which leads to desensitization of the ...
L Y, Jan, Y N, Jan
openaire   +2 more sources

New sites of action for GIRK and SK channels

Nature Reviews Neuroscience, 2009
It was recently discovered that two different types of voltage-insensitive K+ channels, G protein-coupled inwardly rectifying K+ (GIRK) and small-conductance Ca2+-activated K+ (SK) channels, are located on dendritic branches, spines and shafts in the postsynaptic densities of excitatory synapses in many central neurons.
Rafael, Luján   +2 more
openaire   +2 more sources

Structural Insights into GIRK Channel Function

2015
G protein-gated inwardly rectifying potassium (GIRK; Kir3) channels, which are members of the large family of inwardly rectifying potassium channels (Kir1-Kir7), regulate excitability in the heart and brain. GIRK channels are activated following stimulation of G protein-coupled receptors that couple to the G(i/o) (pertussis toxin-sensitive) G proteins.
Ian W, Glaaser, Paul A, Slesinger
openaire   +2 more sources

GIRK Channel Plasticity and Implications for Drug Addiction

2015
Drugs of abuse can "hijack" synaptic plasticity, a physiological basis of learning and memory, establishing maladaptations that can promote drug addiction. A wealth of data supports the existence and importance of neuroadaptations in excitatory neurotransmission upon drug exposure.
Ezequiel, Marron Fernandez de Velasco   +2 more
openaire   +2 more sources

Measuring the Modulatory Effects of RGS Proteins on GIRK Channels

2004
Discovery of "regulators of G-protein signaling" (RGS) as GTPase-activating proteins for heterotrimeric G proteins has provided a highly sought "missing link," reconciling past discrepancies between the in vitro GTPase activity of purified G proteins and the kinetics of physiological responses mediated by G-protein signaling in vivo. With the number of
Craig A, Doupnik   +2 more
openaire   +2 more sources

GIRK Channels

2015
Megan E. Tipps, Kari J. Buck
  +4 more sources

RGS Redundancy and Implications in GPCR–GIRK Signaling

2015
Regulators of G protein signaling (RGS proteins) are key components of GPCR complexes, interacting directly with G protein α-subunits to enhance their intrinsic GTPase activity. The functional consequence is an accelerated termination of G protein effectors including certain ion channels.
openaire   +2 more sources

Localization and Targeting of GIRK Channels in Mammalian Central Neurons

2015
G protein-gated inwardly rectifying K(+) (GIRK/K(ir)3) channels are critical to brain function. They hyperpolarize neurons in response to activation of different G protein-coupled receptors, reducing cell excitability. Molecular cloning has revealed four distinct mammalian genes (GIRK1-4), which, with the exception of GIRK4, are broadly expressed in ...
Rafael, Luján, Carolina, Aguado
openaire   +2 more sources

The Roles of Gβγ and Gα in Gating and Regulation of GIRK Channels

2015
G protein-gated K(+) (GIRK, or Kir3) channels mediate inhibitory neurotransmission via G protein-coupled receptors (GPCRs) in heart and brain. The signaling cascade involves activation of GPCR by an agonist, activation of a G protein followed by rearrangement or dissociation of activated Gα(GTP) from Gβγ, and activation of GIRK by Gβγ.
Nathan, Dascal, Uri, Kahanovitch
openaire   +2 more sources

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