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Juha Voipio

Researcher at University of Helsinki

Publications -  97
Citations -  12296

Juha Voipio is an academic researcher from University of Helsinki. The author has contributed to research in topics: Intracellular pH & Asphyxia. The author has an hindex of 48, co-authored 94 publications receiving 11331 citations. Previous affiliations of Juha Voipio include University of California, Irvine & Helsinki University Central Hospital.

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The K+/Cl- co-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation.

TL;DR: It is shown that, in pyramidal neurons of the rat hippocampus, the ontogenetic change in GABAA-mediated responses from depolarizing to hyperpolarizing is coupled to a developmental induction of the expression of the neuronal Cl−-extruding K+/Cl − co-transporter, KCC2 (ref. 7).
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Cation–chloride co-transporters in neuronal communication, development and trauma

TL;DR: The cation-chloride co-transporters (CCCs) have been identified as important regulators of neuronal Cl- concentration, and recent work indicates that CCCs play a key role in shaping GABA- and glycine-mediated signaling, influencing not only fast cell-to-cell communication but also various aspects of neuronal development, plasticity and trauma.
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Cation-chloride cotransporters in neuronal development, plasticity and disease

TL;DR: This work has shown that one family of ion transporters, cation-chloride cotransporters (CCCs), and in particular K+–Cl− cOTransporter 2 (KCC2), have seminal roles in shaping GABAergic signalling and neuronal connectivity.
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BDNF-induced TrkB activation down-regulates the K+–Cl− cotransporter KCC2 and impairs neuronal Cl− extrusion

TL;DR: It is shown that exposure of rat hippocampal slice cultures and acute slices to exogenous BDNF or neurotrophin-4 produces a TrkB-mediated fall in the neuron-specific K+–Cl− cotransporter KCC2 mRNA and protein, as well as a consequent impairment in neuronal Cl− extrusion capacity.
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Mechanism of Activity-Dependent Downregulation of the Neuron-Specific K-Cl Cotransporter KCC2

TL;DR: It is shown that sustained interictal-like activity in hippocampal slices downregulates KCC2 mRNA and protein expression in CA1 pyramidal neurons, which leads to a reduced capacity for neuronal Cl- extrusion.