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nature neurOSCIenCe VOLUME 13 | NUMBER 10 | OCTOBER 2010 1225 a r t I C l e S

Summary: nature neurOSCIenCe VOLUME 13 | NUMBER 10 | OCTOBER 2010 1225
a r t I C l e S
Neuronal excitability is fundamental to neuronal function and is
primarily controlled by a fine balance between synaptic excitation
and inhibition. In the mammalian CNS, synaptic excitation is chiefly
mediated by the excitatory transmitter glutamate acting on ionotropic
glutamate receptor­gated cationic channels and synaptic inhibition is
primarily mediated by the inhibitory transmitter GABA acting on the
GABAA receptor­gated chloride channel1. In contrast, synaptic inhi-
bition in the brainstem and spinal cord is principally mediated by gly-
cine acting on the glycine receptor (GlyR)-gated chloride channel2,3.
However, in addition to being a primary inhibitory transmitter, gly-
cine can also contribute to excitatory transmission by serving as an
allosteric modulator for the NMDA receptor (NMDAR)4­6.
We found that glutamate and its ligand analogs allosterically poten-
tiated GlyR-mediated currents by interacting with a binding site that
is probably on the subunit of GlyRs. Along with previously demon-
strated glycine potentiation of excitatory NMDA receptors4, our
findings not only blur the traditional distinction between an excita-
tory and an inhibitory transmitter system, but also lead us to propose


Source: Alford, Simon - Department of Biological Sciences, University of Illinois at Chicago


Collections: Biology and Medicine