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Synaptic Regulation of a Thalamocortical Circuit Controls Depression-Related Behavior.

Abstract：

:The NMDA receptor (NMDAR) antagonist ketamine elicits a long-lasting antidepressant response in patients with treatment-resistant depression. Understanding how antagonism of NMDARs alters synapse and circuit function is pivotal to developing circuit-based therapies for depression. Using virally induced gene deletion, ex vivo optogenetic-assisted circuit analysis, and in vivo chemogenetics and fMRI, we assessed the role of NMDARs in the medial prefrontal cortex (mPFC) in controlling depression-related behavior in mice. We demonstrate that post-developmental genetic deletion of the NMDAR subunit GluN2B from pyramidal neurons in the mPFC enhances connectivity between the mPFC and limbic thalamus, but not the ventral hippocampus, and reduces depression-like behavior. Using intersectional chemogenetics, we show that activation of this thalamocortical circuit is sufficient to elicit a decrease in despair-like behavior. Our findings reveal that GluN2B exerts input-specific control of pyramidal neuron innervation and identify a medial dorsal thalamus (MDT)→mPFC circuit that controls depression-like behavior.

journal_name

Cell Rep

journal_title

Cell reports

authors

Miller OH,Bruns A,Ben Ammar I,Mueggler T,Hall BJ

doi

10.1016/j.celrep.2017.08.002

subject

Has Abstract

pub_date

2017-08-22 00:00:00

pages

1867-1880

issue

8

issn

2211-1247

pii

S2211-1247(17)31071-9

journal_volume

20

pub_type

杂志文章

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