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

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 GABAB 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 GABAB receptor-mediated inhibition, respectively. Our data thus provide direct evidence that GABAB 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.

Shao C ，Dong J ，Zhao M ，Liu S ，Wang X ，Yu Y ，Fang L ，Zhu Z ，Chen Q ，Xiao X ，Zhang WN ，Yang K ... -  《-》

GABA releases from parvalbumin-expressing and unspecific GABAergic neurons onto CA1 pyramidal cells are differentially modulated by presynaptic GABA(B) receptors in mouse hippocampus.

Hippocampus CA1 pyramidal cells receive γ-aminobutyric acid (GABA) release from multiple GABAergic interneurons. Combining optogenetic strategy and whole-cell recordings, we demonstrate that baclofen, a specific GABAB receptor agonist, depresses monosynaptic GABAA receptor-mediated transmission from parvalbumin (PV)-expressing interneuron terminals onto pyramidal cells with less efficacy than that from the unspecific GABAergic terminals. The depression from PV neuron terminals is mainly mediated by presynaptic P/N type calcium channels. The results suggest that GABAB receptors are widely expressed on GABAergic interneurons, where they exert inhibition onto pyramidal cells by GABA release with different efficacy. The data strengthen the proposal that diverse GABA neurons play different roles in modulating CA1 pyramidal cell excitability.

Liu Y ，Yang XJ ，Xia H ，Tang CM ，Yang K ... -  《-》

Mu opioid receptors inhibit GABA release from parvalbumin interneuron terminals onto CA1 pyramidal cells.

Selectively activating (by optogenetics) parvalbumin-expressing (PV) interneurons induces GABA release onto CA1 pyramidal cells. Here we report that this release was attenuated by presynaptic mu opioid receptors (MORs) activation. On the other hand, conventional electric shock, presumably activating non-selectively presynaptic GABAergic terminals, also induced GABA release; however, this release showed relatively limited depression by MORs activation. The data suggest that MORs specifically inhibit GABA release from PV terminals and therefore, further support the idea that MORs contribute to homeostasis in CA1 neuro-circuit.

Shao C ，Chen P ，Chen Q ，Zhao M ，Zhang WN ，Yang K ... -  《-》

Requirement for CB1 but not GABAB receptors in the cholecystokinin mediated inhibition of GABA release from cholecystokinin expressing basket cells.

Lee SH ，Soltesz I 《-》

Differential surface density and modulatory effects of presynaptic GABA(B) receptors in hippocampal cholecystokinin and parvalbumin basket cells.

Booker SA ，Althof D ，Degro CE ，Watanabe M ，Kulik Á ，Vida I ... -  《-》