Journal
EUROPEAN JOURNAL OF NEUROSCIENCE
Volume 21, Issue 9, Pages 2593-2599Publisher
WILEY
DOI: 10.1111/j.1460-9568.2005.04084.x
Keywords
Ca2+ cortex; depolarization; development
Categories
Funding
- NIDCD NIH HHS [R01 DC004199] Funding Source: Medline
- NINDS NIH HHS [R56 NS043277, R01 NS043277-10, R01 NS043277-02, NS43277, R01 NS043277, NS29365] Funding Source: Medline
- PHS HHS [04199] Funding Source: Medline
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During brain development, GABA and glycine switch from being depolarizing to being hyperpolarizing neurotransmitters. This conversion results from a gradual decrease in the chloride electrochemical equilibrium potential (E-Cl) of developing neurons, which correlates to an increase in the expression or activity of the potassium chloride cotransporter, KCC2. However, evidence as to whether KCC2 expression is sufficient, in and of itself, to induce this switch is lacking. In order to address this question, we used a gain-of-function approach by over-expressing human KCC2 (hKCC2) in immature cortical neurons, before endogenous up-regulation of KCC2. We found that premature expression of hKCC2 produced a substantial negative shift in the GABA reversal potential and decreased or abolished GABA-elicited calcium responses in cultured neurons. We conclude that KCC2 expression is not only necessary but is also sufficient for ending the depolarizing period of GABA in developing cortical neurons.
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