File Download

There are no files associated with this item.

  • Find it @ UNIST can give you direct access to the published full text of this article. (UNISTARs only)
Related Researcher


Kim, Jae-Ick
Neural Circuit and Neurodegenerative Disease Lab.
Read More

Views & Downloads

Detailed Information

Cited time in webofscience Cited time in scopus
Metadata Downloads

Deletion of PLCγ1 in GABAergic Neurons Leads to Spontaneous Seizure in Mice

Kim, Hye YunYang, Yong RyoulHwang, HongikJang, Hyun-JunKim, JeongyeonYang, EstherKim, HyunRhim, HyewhonKim, Jae-IckSuh, Pann-Ghill
Issued Date
2019 International Conference: Korean Society for Molecular and Cellular Biology
Excitation/inhibition (E/I) balance plays a fundamental role in information processing of neural circuits. It coordinates various neural functions and dysregulated E/I balance causes multiple neurological disorders. Among them, epilepsy is associated with hyperexcitability of neurons caused by the deficits of GABAergic neuron or decreased GABAergic inhibition at synapses. Although many antiepileptic drugs are intended to improve GABAmediated inhibition via GABAergic interneurons, molecular mechanisms of E/I balance regulated by GABAergic neurons are not fully understood. Increasing evidence indicates that phospholipase C γ1 (PLCγ1) is involved in the generation of seizure, while the causal relationship between PLCγ1 and seizure has not been firmly established. Here, we show that genetic deletion of PLCγ1 in GABAergic neurons leads to spontaneous seizure. Plcg1F/F;Dlx5/6-Cre mice also exhibits other behavioral alterations, including hypoactivity, reduced anxiety, and fear memory deficit. Notably, inhibitory synaptic transmission as well as the number of inhibitory synapses are decreased in hippocampus. These findings suggest that PLCγ1 may be a key determinant of maintaining both inhibitory synapses and synaptic transmission, potentially contributing to the regulation of E/I balance in hippocampus.
Korean Society for Molecular and Cellular Biology


Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.