The γ2 subunit of GABAA receptor chloride channels is required for normal channel function and for postsynaptic clustering of these receptors during synaptogenesis. In addition, GABAA receptor function is thought to contribute to normal postnatal maturation of neurons. Loss of postsynaptic GABAA receptors in γ2-deficient neurons might therefore reflect a deficit in maturation of neurons due to the reduced channel function. Here, we have used the Cre-loxP strategy to examine the clustering function of the γ2 subunit at mature synapses. Deletion of the γ2 subunit in the third postnatal week resulted in loss of benzodiazepine-binding sites and parallel loss of punctate immunoreactivity for postsynaptic GABAA receptors and gephyrin. Thus, the γ2 subunit contributes to postsynaptic localization of GABAA receptors and gephyrin by a mechanism that is operant in mature neurons and not limited to immature neurons, most likely through interaction with proteins involved in trafficking of synaptic GABAA receptors.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cellular and Molecular Neuroscience
- Cell Biology