RT Journal Article
SR Electronic
T1 Input-specific NMDAR-dependent potentiation of dendritic GABAergic inhibition
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 155077
DO 10.1101/155077
A1 Chiayu Q. Chiu
A1 James S. Martenson
A1 Maya Yamazaki
A1 Rie Natsume
A1 Kenji Sakimura
A1 Susumu Tomita
A1 Steven J. Tavalin
A1 Michael J. Higley
YR 2017
UL http://biorxiv.org/content/early/2017/06/24/155077.abstract
AB Preservation of a balance between synaptic excitation and inhibition is critical for normal brain function. A number of homeostatic cellular mechanisms have been suggested to play a role in maintaining this balance, including long-term plasticity of GABAergic inhibitory synapses. Many previous studies have demonstrated a coupling of postsynaptic spiking with modification of perisomatic inhibition. Here, we demonstrate that activation of NMDA-type glutamate receptors leads to input-specific long-term potentiation of dendritic inhibition mediated by somatostatin-expressing interneurons. This form of plasticity is expressed postsynaptically and requires both CaMKIIα and the β2-subunit of the GABA-A receptor. Importantly, this process may function to preserve dendritic inhibition, as in vivo loss of NMDAR signaling results in a selective weakening of dendritic inhibition. Overall, our results reveal a new mechanism for linking excitatory and inhibitory input in neuronal dendrites and provide novel insight into the homeostatic regulation of synaptic transmission in cortical circuits.