PT  - JOURNAL ARTICLE
AU  - Chiayu Q. Chiu
AU  - James S. Martenson
AU  - Maya Yamazaki
AU  - Rie Natsume
AU  - Kenji Sakimura
AU  - Susumu Tomita
AU  - Steven J. Tavalin
AU  - Michael J. Higley
TI  - Input-specific NMDAR-dependent potentiation of dendritic GABAergic inhibition
AID  - 10.1101/155077
DP  - 2017 Jan 01
TA  - bioRxiv
PG  - 155077
4099  - http://biorxiv.org/content/early/2017/06/24/155077.short
4100  - http://biorxiv.org/content/early/2017/06/24/155077.full
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.