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Verfasst von:Titz, Stefan [VerfasserIn]   i
 Hormuzdi, Sheriar [VerfasserIn]   i
 Lewen, Andrea [VerfasserIn]   i
 Monyer, Hannah [VerfasserIn]   i
 Misgeld, Ulrich [VerfasserIn]   i
Titel:Intracellular acidification in neurons induced by ammonium depends on KCC2 function
Verf.angabe:Stefan Titz, Sheriar Hormuzdi, Andrea Lewen, Hannah Monyer and Ulrich Misgeld
E-Jahr:2006
Jahr:18 January 2006
Umfang:11 S.
Teil:volume:23
 year:2006
 number:2
 pages:454-464
 extent:11
Fussnoten:Gesehen am 07.04.2021
Titel Quelle:Enthalten in: European journal of neuroscience
Ort Quelle:Oxford [u.a.] : Wiley, 1989
Jahr Quelle:2006
Band/Heft Quelle:23(2006), 2, Seite 454-464
ISSN Quelle:1460-9568
Abstract:The Cl--extruding neuron-specific K+-Cl- cotransporter KCC2, which establishes hyperpolarizing inhibition, can transport NH4+ instead of K+. It is, however, not clear whether KCC2 provides the only pathway for neuronal NH4+ uptake. We therefore investigated NH4+ uptake in cultured rat brain neurons. In neurons cultured for > 4 weeks, the response to NH4Cl applications (5 mm) consisted of an alkaline shift which reversed to an acid shift within seconds. Rebound acid shifts which followed brief applications of NH4Cl were blocked by furosemide (100 µm). They were rather insensitive to bumetanide (1 and 100 µm), in contrast to those induced in cultured glial cells. Rebound acid shifts persisted in the presence of 1 mm Ba2+ and in Na+-free solution but were inhibited by extracellular K+. In neurons with depolarizing GABA responses, indicating the absence of functional KCC2, applications of NH4Cl barely induced an acidosis. However, large rebound acid shifts occurred in neurons that had changed their GABA response from Ca2+ increases to Ca2+ decreases. Rebound acid shifts continued to increase even after the change in the GABA response had occurred and could be induced earlier in neurons transfected with KCC2 cDNA. We conclude that KCC2 provides the main pathway for fast neuronal NH4+ uptake. Therefore, NH4Cl-induced rebound acid shifts can be used to indicate the development of KCC2 function. Further, the well known up-regulation of KCC2 function during development has the inevitable consequence of opening a major pathway for NH4+ influx, which can be relevant under pathophysiological conditions.
DOI:doi:10.1111/j.1460-9568.2005.04583.x
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/https://doi.org/10.1111/j.1460-9568.2005.04583.x
 Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1460-9568.2005.04583.x
 DOI: https://doi.org/10.1111/j.1460-9568.2005.04583.x
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:development
 GABA
 NKCC1
 rat cultured neurons
 synaptic inhibition
K10plus-PPN:1753252407
Verknüpfungen:→ Zeitschrift

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