| First Author | Giugovaz-Tropper B | Year | 2011 |
| Journal | Neuroscience | Volume | 192 |
| Pages | 219-30 | PubMed ID | 21718757 |
| Mgi Jnum | J:176694 | Mgi Id | MGI:5292445 |
| Doi | 10.1016/j.neuroscience.2011.06.021 | Citation | Giugovaz-Tropper B, et al. (2011) P/Q-type calcium channel ablation in a mice glycinergic synapse mediated by multiple types of Ca(2)+ channels alters transmitter release and short term plasticity. Neuroscience 192:219-30 |
| abstractText | Ca(v)2.1 channels (P/Q-type) play a prominent role in controlling neurotransmitter release. Transgenic mice in which the alpha1A pore-forming subunit of Ca(v)2.1 channels is ablated (KO) provide a powerful tool to study Ca(v)2.1 function in synaptic transmission in vivo. Whole-cell patch clamp was used to measure inhibitory glycinergic postsynaptic currents (IPSCs) from the lateral superior olive (LSO). Comparing wild-type (WT) and KO mice, we investigated the relevance of P/Q-type calcium channels at a glycinergic synapse mediated by multiple types of Ca(2+) channels, in opposition to synapses where only this type of Ca(2+) channels are in charge of transmitter release. We found that in KO mice, N-type and L-type Ca(2+) channels control synaptic transmission, resulting in a functional but reduced glycinergic transmitter release. Pair pulse facilitation of synaptic currents is retained in KO mice, even when synaptic transmission is driven by either N or L-type calcium channels alone, in contrast with lack of this phenomenon in other synapses which are exclusively mediated by P/Q-type channels. Thus, pointing a difference between P/Q- and N-type channels present in single or multiple types of calcium channels driven synapses. Significant alterations in short-term synaptic plasticity were observed. KO mice exhibited a stronger short term depression (STD) of IPSCs during repetitive stimulation at high frequency and recovered with a larger time constant compared to WT mice. Finally, transmitter release at the LSO synapse from KO mice was strongly modulated by presynaptic GTP-binding protein-coupled receptor gamma-aminobutyric acid type B (GABA(B)). |
