Journal
NEURON
Volume 97, Issue 2, Pages 368-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2017.12.032
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Funding
- NIH [R01 MH099045, R01 NS076637, R01 MH115705, F30 MH099742, K01 MH097961]
- March of Dimes Basil O'Connor Award
- FONDECYT [1171840]
- MILENIO PROYECTO [P09-022-F]
- CINV
- Grants-in-Aid for Scientific Research [25000015, 17K19444, 16H06276] Funding Source: KAKEN
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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 CaMKII alpha and the beta 2 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.
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