Abstract：
:Functional neural circuit formation during development involves massive elimination of redundant synapses. In the cerebellum, one-to-one connection from excitatory climbing fiber (CF) to Purkinje cell (PC) is established by elimination of early-formed surplus CFs. This process depends on glutamatergic excitatory inputs, but contribution of GABAergic transmission remains unclear. Here, we demonstrate impaired CF synapse elimination in mouse models with diminished GABAergic transmission by mutation of a single allele for the GABA synthesizing enzyme GAD67, by conditional deletion of GAD67 from PCs and GABAergic interneurons or by pharmacological inhibition of cerebellar GAD activity. The impaired CF synapse elimination was rescued by enhancing GABA(A) receptor sensitivity in the cerebellum by locally applied diazepam. Our electrophysiological and Ca2+ imaging data suggest that GABA(A) receptor-mediated inhibition onto the PC soma from molecular layer interneurons influences CF-induced Ca2+ transients in the soma and regulates CF synapse elimination from postnatal day 10 (P10) to around P16.
journal_name
Neuronjournal_title
Neuronauthors
Nakayama H,Miyazaki T,Kitamura K,Hashimoto K,Yanagawa Y,Obata K,Sakimura K,Watanabe M,Kano Mdoi
10.1016/j.neuron.2012.02.032subject
Has Abstractpub_date
2012-04-26 00:00:00pages
384-96issue
2eissn
0896-6273issn
1097-4199pii
S0896-6273(12)00269-3journal_volume
74pub_type
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