| First Author | Riazanski V | Year | 2011 |
| Journal | Nat Neurosci | Volume | 14 |
| Issue | 4 | Pages | 487-94 |
| PubMed ID | 21378974 | Mgi Jnum | J:172302 |
| Mgi Id | MGI:5006894 | Doi | 10.1038/nn.2775 |
| Citation | Riazanski V, et al. (2011) Presynaptic CLC-3 determines quantal size of inhibitory transmission in the hippocampus. Nat Neurosci 14(4):487-94 |
| abstractText | The absence of the chloride channel CLC-3 in Clcn3(-/-) mice results in hippocampal degeneration with a distinct temporal-spatial sequence that resembles neuronal loss in temporal lobe epilepsy. We examined how the loss of CLC-3 might affect GABAergic synaptic transmission in the hippocampus. An electrophysiological study of synaptic function in hippocampal slices taken from Clcn3(-/-) mice before the onset of neurodegeneration revealed a substantial decrease in the amplitude and frequency of miniature inhibitory postsynaptic currents compared with those in wild-type slices. We found that CLC-3 colocalized with the vesicular GABA transporter VGAT in the CA1 region of the hippocampus. Acidification of inhibitory synaptic vesicles induced by Cl(-) showed a marked dependence on CLC-3 expression. The decrease in inhibitory transmission in Clcn3(-/-) mice suggests that the neurotransmitter loading of synaptic vesicles was reduced, which we attribute to defective vesicular acidification. Our observations extend the role of Cl(-) in inhibitory transmission from that of a postsynaptic permeant species to a presynaptic regulatory element. |
