Gyu Park's research while affiliated with Virginia Commonwealth University and other places

... Immunoprecipitation studies were performed to evaluate whether the 5-HT 2A and the mGlu2/3 receptor proteins physically associate in PFc synaptosomes. We focused on the mGlu2 subunit protein since previous studies showed that this is the subunit which preferentially interacts with 5-HT 2A receptor proteins by means of specific aminoacid(s) [12,[30][31][32]. The lysates of PFc synaptosomes were immunoprecipitated with an antibody recognizing the mGlu2 receptor protein (Figure 3a), or with an antibody recognizing the 5-HT 2A receptor protein (Figure 3b). ...

... Pharmacology, Biochemistry and Behavior 175 (2018) [89][90][91][92][93][94][95][96][97][98][99][100] studies showing that extended access to self-administered meth and 7 days of withdrawal alters synaptic plasticity and mGlu expression in the PRh Scofield et al., 2015), produces PRh/ dHPC-dependent memory deficits , dysregulates 5-HT levels (Brennan et al., 2010) and glutamate neurophysiology in the PFC (Mishra et al., 2016). As the functional (and behavioral) outcome of the 5-HT2A and mGlu2 interaction depends on the relative amount of each receptor (Baki et al., 2013), the 5-HT2A/mGlu2 protein expression ratio was also calculated. Extended access to meth upregulated 5-HT2A protein levels in the mPFC [t(9) = 2.96, p < 0.05] and the PRh [t (9) = 2.61, p < 0.05] compared to yoked-saline rats. ...

... In addition to presynaptically controlling glutamate exocytosis, mGlu2/3 receptors were also reported to colocalize and functionally crosstalk with 5-HT 2A receptors, contributing to an integrated "metamodulation" of synaptic transmission [8][9][10]. This interaction was first described in the mammal cortex, where the 5-HT 2A receptors and mGlu2 receptors were shown to physically associate in a heterodimeric complex at the postsynaptic level [11][12][13][14]. The two receptors were proposed to crosstalk in an antagonist fashion, based on the finding that the pharmacological antagonism of mGlu2/3 receptors potentiated the spontaneous excitatory postsynaptic currents elicited by 5-HT 2A receptors, whereas mGlu2/3 agonists reduced their expression and functions [15][16][17][18]. ...