Fig. 3.

HNK-1 on GluA2 regulates its synaptic membrane residency and spine maturation process. a A glutamate receptor subunit, GluA2, interacts with N-cadherin at the postsynaptic membrane. In GlcAT-P knockout neurons, loss of HNK-1 on GluA2 results in weaker interaction with N-cadherin and enhanced internalization of GluA2. This phenomenon could be one mechanism behind the reduced long-term potentiation in GlcAT-P knockout neurons. b In GlcAT-P knockout neurons, immature thin spines are observed. Also, loss of HNK-1 on GluA2 changes its localization from spines to dendritic shafts