Results 191 to 200 of about 4,475 (201)
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CIP1 is an activator of the K+–Cl− cotransporter KCC2

Biochemical and Biophysical Research Communications, 2009
In most neurons, efficient setting of the intracellular Cl(-)-concentration requires the coordinated regulation of the Cl(-)-inward transporter NKCC1 and the Cl(-)-outward transporter KCC2. Previously, the cation-chloride cotransporter interacting protein 1 (CIP1) was shown to inactivate NKCC1. Here, we investigated its role for KCC2 activity. After co-
Anna-Maria Hartmann   +3 more
openaire   +3 more sources

Behavioural phenotypes of hypomorphic KCC2‐deficient mice

European Journal of Neuroscience, 2005
AbstractHyperpolarizing fast inhibitory neurotransmission by γ‐aminobutyric acid and glycine requires an efficient chloride extrusion mechanism in postsynaptic neurons. A major effector of this task in adult animals is the potassium‐chloride co‐transporter KCC2 that is selectively and abundantly expressed postsynaptically in most CNS neurons.
Heikki Rauvala   +4 more
openaire   +3 more sources

The KCC2 Cotransporter and Human Epilepsy

The Neuroscientist, 2016
The cation-Cl− cotransporter KCC2, encoded by SLC12A5, is required for the emergence and maintenance of GABAergic fast synaptic inhibition in organisms across evolution. These findings have suggested that KCC2 deficiency might play a role in the pathogenesis human epilepsy, but this has only recently been substantiated by two lines of genetic evidence.
Arjun Khanna   +5 more
openaire   +3 more sources

Implication of KCC2 in the sensitization to morphine by chronic ethanol treatment in mice

Synapse, 2013
Chronic consumption of ethanol has been reported to modify several molecular events in the central nervous system (CNS). Ethanol directly or indirectly stimulates mesolimbic dopaminergic neurons and increases the release of dopamine in the nucleus accumbens (NAc; Xiao et al., 2007).
Tomohisa Tsuyuki   +8 more
openaire   +3 more sources

Seizing Control of KCC2: A New Therapeutic Target for Epilepsy

Trends in Neurosciences, 2017
Deficits in GABAergic inhibition result in the abnormal neuronal activation and synchronization that underlies seizures. However, the molecular mechanisms responsible for transforming a normal brain into an epileptic one remain largely unknown. Hyperpolarizing inhibition mediated by type A GABA (GABAA) receptors is dependent on chloride extrusion by ...
Stephen J. Moss   +6 more
openaire   +3 more sources

Quest for pharmacological regulators of KCC2

2020
Davide Pozzi, Bice Chini
openaire   +1 more source

Intracellular taurine inhibits KCC2 transporter activity

Neuroscience Research, 2010
Atsuo Fukuda   +5 more
openaire   +2 more sources

KCC2

2009
openaire   +1 more source

KCC2 is a hub protein that balances excitation and inhibition

2020
Jessica C. Pressey   +2 more
openaire   +1 more source

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