First Author | Chiu CQ | Year | 2018 |
Journal | Neuron | Volume | 97 |
Issue | 2 | Pages | 368-377.e3 |
PubMed ID | 29346754 | Mgi Jnum | J:255317 |
Mgi Id | MGI:6114331 | Doi | 10.1016/j.neuron.2017.12.032 |
Citation | Chiu CQ, et al. (2018) Input-Specific NMDAR-Dependent Potentiation of Dendritic GABAergic Inhibition. Neuron 97(2):368-377.e3 |
abstractText | 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 CaMKIIalpha and the beta2 subunit of the GABA-A receptor. Importantly, this process may function to preserve dendritic inhibition, as genetic deletion 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. |