Impaired fast-spiking interneuron function in a genetic mouse model of depression

ELife
Jonas-Frederic SauerMarlene Bartos

Abstract

Rhythmic neuronal activity provides a frame for information coding by co-active cell assemblies. Abnormal brain rhythms are considered as potential pathophysiological mechanisms causing mental disease, but the underlying network defects are largely unknown. We find that mice expressing truncated Disrupted-in-Schizophrenia 1 (Disc1), which mirror a high-prevalence genotype for human psychiatric illness, show depression-related behavior. Theta and low-gamma synchrony in the prelimbic cortex (PrlC) is impaired in Disc1 mice and inversely correlated with the extent of behavioural despair. While weak theta activity is driven by the hippocampus, disturbance of low-gamma oscillations is caused by local defects of parvalbumin (PV)-expressing fast-spiking interneurons (FS-INs). The number of FS-INs is reduced, they receive fewer excitatory inputs, and form fewer release sites on targets. Computational analysis indicates that weak excitatory input and inhibitory output of FS-INs may lead to impaired gamma oscillations. Our data link network defects with a gene mutation underlying depression in humans.

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Citations

Feb 10, 2016·Frontiers in Systems Neuroscience·Torfi Sigurdsson, Sevil Duvarci
Feb 3, 2016·Frontiers in Cellular Neuroscience·Olga VoinovaAndrei Rozov
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Nov 16, 2019·International Journal of Bipolar Disorders·Julia AlcaideJuan Nacher
May 16, 2020·Frontiers in Neuroscience·Aurore BrunetCaroline Rouaux
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Jul 17, 2020·The European Journal of Neuroscience·Ismary Blanco, Katherine Conant
Sep 25, 2021·Psychiatry and Clinical Neurosciences·Yoji Hirano, Peter J Uhlhaas

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Software Mentioned

MTrack2
Python
Chronux toolbox
Learning Analysis
MATLAB
ImageJ
NEURON

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