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This
paper describes a novel repressor element site in the 5«region (RE-1)
of the Kcc2b gene which encodes the KCC2 potassium-chloride
co-transporter. This transporter is required for the inhibitory
action of the neurotransmitter gamma-aminobutyric acid (GABA). Thus,
RE-1 functions as a novel transcription brake for KCC2 expression
explaining why developing neurons and the prenatal brain are in a
hyperexcitatory state.
At birth, the brain undergoes a
developmental shift, e.g. loss of this hyperexcitability by inhibition
of the KCC2-transcription break, a necessary step for normal brain
development which now enables GABA to function as an inhibitory
transmitter. This is a fundamental mechanism for brain function.
However, it remains unknown how the brakes are turned off so Kcc2b
can encode for the transporter proteins. These findings are important
for brain development and may also explain neuronal ÒmisfiringÓ which
leads to diseases like epilepsy and chronic pain.
Competing interests: None
declared
Evaluated 24 Nov 2009
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New
Finding