Tat-NR2BAA is an inactive control peptide of Tat-NR2B9c. It shares a similar sequence with Tat-NR2B9c, but possesses a double-point mutation in the COOH terminal tSXV motif. This mutation renders Tat-NR2BAA unable to bind PSD-95. Tat-NR2B9c, on the other hand, is a membrane-permeable peptide that interferes with PSD-95/NMDAR binding. This interference leads to the decoupling of NR2B- and/or NR2A-type NMDARs from PSD-95[1][2].

Tat-NR2BAA (125 ng; 20 mins) does not affect the interaction between PSD-95 and NR2B subunits. Conversely, the interaction is significantly reduced in rats pre-treated with Tat-NR2B9c in the lumbar dorsal horn tissue, as evidenced by coimmunoprecipitation results[1]. As a control, Tat-NR2Baa (125 ng or 1.25 μg; 20 minutes before tissue collection) does not influence these interactions, even at doses 100 times greater than the effective Tat-NR2B9c[1]. Moreover, Tat-NR2Baa (1 μM; pre-treatment 1 hour) serves as the control in a co-immunoprecipitation assay where Tat-NR2B9c (1 μM) specifically disrupts the NR2B/PSD-95 interaction. This disruption indicates the enhanced sensitivity of NR2B/PSD-95 coupling compared to NR2A/PSD-95 in hippocampal neurons, with Tat-NR2B9c leading to a significant reduction in post-discharge, highlighting cellular hyperexcitability[2].