Synaptic transmission efficacy can be bi-directionally modified through potentiation (long-term potentiation (LTP)) or depression (long-term depression (LTD)) as well as the phosphorylation state of Ser831 and Ser845 sites at the GluA1 subunit of the glutamate AMPA receptors, which has been characterized as a critical event for this synaptic plasticity.
The (2R,6R)-HNK concentrations that increased GluA1 expression are consistent with its maximal C<sub>b,u</sub> (0.92-4.84 μM) at reportedly efficacious doses of ketamine or (2R,6R)-HNK in mouse depression models, but ≥3-fold above its projected maximal human C<sub>b,u</sub> (≤37.8 ± 14.3 nM) following ketamine's clinically antidepressant infusion.
Our data indicate that capsaicin-induced modulation of LA-LTP via TRPV1 involves GluA1-containing AMPARs whereas capsaicin-induced modulation of LA-LTD via TRPM1 is independent of the expression of the AMPAR GluA1 subunit.
Our study reveals that the CTDs of GluA1 and GluA2, the key subunits of AMPARs, are necessary and sufficient to drive NMDA receptor-dependent LTP and LTD, respectively.
Here we show that tamoxifen-induced GluA1 deletion restricted to forebrain glutamatergic neurons of post-adolescent mice does not induce depression- and anxiety-like changes.
Here we show that tamoxifen-induced GluA1 deletion restricted to forebrain glutamatergic neurons of post-adolescent mice does not induce depression- and anxiety-like changes.
Our results provide evidence for a significant role of hippocampal GluA1-containing AMPA receptors and their PDZ-interaction in experience-dependent expression of behavioral despair and link mechanisms of hippocampal synaptic plasticity with behavioral expression of depression.
We examined whether polymorphisms in the GRIK2, GRIA3 and GRIA1 genes were associated with selective serotonin reuptake inhibitor (SSRI)-associated sexual dysfunction in 114 participants treated for depression.