Disinhibition of somatostatin-positive interneurons by deletion of postsynaptic GABAA receptors.
Disinhibition of somatostatin-positive interneurons by deletion of postsynaptic GABAA receptors.
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DOI：
10.1038/mp.2017.110
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发表时间：
2017-06-01
影响因子：
11
通讯作者：
Luscher, B
中科院分区：
文献类型：
--
作者：
Fuchs, T;Jefferson, S J;Luscher, B
Legend: Fuchs and Jefferson et al. used selective deletion of the γ2 subunit of GABAA receptors from somatostatin-positive GABAergic interneurons to disinhibit these neurons and, in turn, to increase GABAergic synaptic input to principal target cells. The mutant mice mimicked the behavioral and biochemical alterations reminiscent of rapidly acting antidepressants such as ketamine, suggesting that selectively increasing the activity of somatostatin-positive interneurons might serve as a novel strategy for antidepressant therapies. Images represent optical sections of a somatostatin-positive interneuron of a control (left) and mutant brain (right) immunostained for the γ2 subunit (green) and the subsynaptic scaffolding protein, gephyrin (red), with the soma labeled in blue. Note the loss of punctate staining for both markers, indicative of loss of inhibitory synaptic input to these cells. For more information on this topic, please refer to the article by Fuchs et al. on pages 920–930.
