Abstract:
:We identified four PDZ domain-containing proteins, syntenin, PICK1, GRIP, and PSD95, as interactors with the kainate receptor (KAR) subunits GluR5(2b,) GluR5(2c), and GluR6. Of these, we show that both GRIP and PICK1 interactions are required to maintain KAR-mediated synaptic function at mossy fiber-CA3 synapses. In addition, PKC alpha can phosphorylate ct-GluR5(2b) at residues S880 and S886, and PKC activity is required to maintain KAR-mediated synaptic responses. We propose that PICK1 targets PKC alpha to phosphorylate KARs, causing their stabilization at the synapse by an interaction with GRIP. Importantly, this mechanism is not involved in the constitutive recycling of AMPA receptors since blockade of PDZ interactions can simultaneously increase AMPAR- and decrease KAR-mediated synaptic transmission at the same population of synapses.
journal_name
Neuronjournal_title
Neuronauthors
Hirbec H,Francis JC,Lauri SE,Braithwaite SP,Coussen F,Mulle C,Dev KK,Coutinho V,Meyer G,Isaac JT,Collingridge GL,Henley JMdoi
10.1016/s0896-6273(02)01191-1subject
Has Abstractpub_date
2003-02-20 00:00:00pages
625-38issue
4eissn
0896-6273issn
1097-4199pii
S0896627302011911journal_volume
37pub_type
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