Presynaptic GABAB receptors differentially modulate GABA release from cholecystokinin and parvalbumin interneurons onto CA1 pyramidal neurons: A cell type-specific labeling and activating study

被引:6
|
作者
Shao, Caifeng [1 ,2 ]
Dong, Jiaxue [2 ]
Zhao, Mingwei [2 ]
Liu, Shenhao [3 ]
Wang, Xue [3 ]
Yu, Yang [3 ]
Fang, Lingyan [3 ]
Zhu, Ziying [2 ]
Chen, Qian [2 ]
Xiao, Xu [4 ]
Zhang, Wei-Ning [4 ]
Yang, Kun [2 ,5 ]
机构
[1] Nanjing Univ Tradit Chinese Med, Nantong Hosp, Nantong Hosp Tradit Chinese Med, Dept Anesthesiol, Nantong 226001, Jiangsu, Peoples R China
[2] Jiangsu Univ, Sch Med, Dept Anat, Zhenjiang 212013, Jiangsu, Peoples R China
[3] Jiangsu Univ, Sch Med, Clin Med Class 1907, Zhenjiang 212013, Jiangsu, Peoples R China
[4] JiangsuUniv, Sch Med, Dept Pathophysiol, Zhenjiang 212013, Jiangsu, Peoples R China
[5] Univ Maryland, Sch Med, Dept Neurol, Baltimore, MD 21201 USA
基金
中国国家自然科学基金;
关键词
Hippocampus; Cholecystokinin; Parvalbumin; GABA; GABA(B) receptors; Optogenetics;
D O I
10.1016/j.neulet.2022.136448
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Combining cell type-specific optogenetics and whole cell recordings on mouse acute hippocampal slices, we compared GABA release from cholecystokinin-expressing (CCK) and parvalbumin-expressing (PV) interneurons onto CA1 pyramidal neurons. Baclofen, a selective GABA(B) receptor agonist, inhibited GABAergic synaptic transmission greater from CCK terminals, compared to that from PV terminals. The N-type calcium channels on CCK and P/Q-type calcium channels on PV terminals contributed to the GABA(B) receptor-mediated inhibition, respectively. Our data thus provide direct evidence that GABA(B) receptors differentially modulate GABA release from CCK and PV interneurons, adding to an increasing list of differences between these two interneuron subtypes in modulating hippocampal pyramidal neurons.
引用
收藏
页数:4
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