A distinct form of hippocampal long term depression (LTD) is induced by activation of group I metabotropic glutamate receptors (mGluRs) by the specific agonist dihydroxyphenylglycine (DHPG)¹. AMPA receptor redistribution has been implicated in this form of LTD. Also the AMPA receptor subunit GluR2 is transiently dephosphorylated in response to DHPG via a protein tyrosine phosphatase (PTP)². The mechanism of AMPA receptor redistribution is not fully understood however. Here we have used a super ecliptic pHluorin tagged version of GluR2 (SEP-GluR2) to study this phenomenon³. 14 day old postnatal hippocampal cultured neurones were infected with SEP-GluR2 using the sindbis virus. 17-24 hours later these neurones were used in experiments. SEP-GluR2 infected neurones show a reduction in mEPSC frequency upon DHPG application that is comparable to that seen in non-infected neurones (76±2% of pre-DHPG frequency). The mEPSC amplitude was unaffected. In addition we found that 30 minutes after DHPG application the fluorescence from surface expressed SEP-GluR2 was significantly decreased to 83±6% of pre-DHPG values. The DHPG induced decrease in surface SEP-GluR2 was prevented when DHPG was applied in the presence of either the mGluR5 antagonist MPEP (93±10% of control) or the PTP inhibitor orthovanadate (100±7% of control). In summary, by using live cell imaging we have found that DHPG causes a reduction in surface SEP-GluR2 containing AMPA receptors.