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PLoS Biol. 2014 Jul 8;12(7):e1001903. doi: 10.1371/journal.pbio.1001903. eCollection 2014 Jul.

Non-associative potentiation of perisomatic inhibition alters the temporal coding of neocortical layer 5 pyramidal neurons.

Author information

1
European Brain Research Institute, Rome, Italy; Sorbonne Universités UPMC Univ. Paris 06, UMR S 1127, Paris, France; Inserm U 1127, Paris, France; CNRS UMR 7225, Paris, France; ICM- Institut du Cerveau et de la Moelle épinière, Paris, France.
2
European Brain Research Institute, Rome, Italy.
3
CNRS UMR 3571, Paris, France; Institut Pasteur, Unit of Dynamic Neuronal Imaging, Paris, France.

Abstract

In the neocortex, the coexistence of temporally locked excitation and inhibition governs complex network activity underlying cognitive functions, and is believed to be altered in several brain diseases. Here we show that this equilibrium can be unlocked by increased activity of layer 5 pyramidal neurons of the mouse neocortex. Somatic depolarization or short bursts of action potentials of layer 5 pyramidal neurons induced a selective long-term potentiation of GABAergic synapses (LTPi) without affecting glutamatergic inputs. Remarkably, LTPi was selective for perisomatic inhibition from parvalbumin basket cells, leaving dendritic inhibition intact. It relied on retrograde signaling of nitric oxide, which persistently altered presynaptic GABA release and diffused to inhibitory synapses impinging on adjacent pyramidal neurons. LTPi reduced the time window of synaptic summation and increased the temporal precision of spike generation. Thus, increases in single cortical pyramidal neuron activity can induce an interneuron-selective GABAergic plasticity effectively altering the computation of temporally coded information.

PMID:
25003184
PMCID:
PMC4086817
DOI:
10.1371/journal.pbio.1001903
[Indexed for MEDLINE]
Free PMC Article

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